Germline genetic variants may help explain why CAR T cell therapy produces such variable toxicity across patients with aggressive lymphoma, according to findings published in Science Immunology.1 Investigators identified a specific gene, STXBP2, whose variants were enriched among patients who developed severe toxicity after treatment with axicabtagene ciloleucel.

"CAR T cells are different than every other form of therapy that came before," said Mark B. Leick, MD, medical oncologist and physician-scientist at Massachusetts General Hospital and the study's corresponding author. Unlike a standardized drug, Leick noted, CAR T cells are manufactured from a patient's own T cells, carrying all of that patient's inherited genetic variation into the final product.

A Genetic Signature May Predict Who Gets Sick From CAR T Cell Therapy

A Rare Disease Pointed Investigators Toward STXBP2

Investigators performed whole genome sequencing on patients with aggressive lymphoma treated with axicabtagene ciloleucel in the ZUMA-1 (n = 86 evaluable) and ZUMA-7 (n = 150 evaluable) clinical trials, in partnership with Kite Pharma.1 The hypothesis was rooted in hemophagocytic lymphohistiocytosis (HLH), a rare inherited hyperinflammatory syndrome that shares key biochemical features with cytokine release syndrome (CRS), the most common toxicity of CAR T cell therapy.1 Leick and colleagues reasoned that milder, adult-onset forms of the same genetic defects that cause HLH might also be driving toxicity in some CAR T cell recipients.

Among the ZUMA-1 toxicity cohort (n = 39), 6 patients (15.4%; 95% CI, 5.9%-30.1%) carried putative deleterious variants in STXBP2, a gene involved in lymphocyte degranulation, compared with none in the 39-patient control cohort (OR, >1.44; nominal P = .025).1 The finding was not replicated in ZUMA-7, which investigators attributed to that cohort's lower baseline inflammation and fewer prior treatments relative to the more heavily pretreated ZUMA-1 population.

CRISPR Experiments Confirmed a Mechanistic Role

To confirm a mechanistic role for the gene, investigators used CRISPR-Cas9 to knock out STXBP2 in CAR T cells manufactured from healthy donors.

The STXBP2-deficient cells showed impaired degranulation and cytotoxicity, along with increased inflammatory cytokine production when cocultured with tumor targets, mirroring the cytokine profile seen in variant carriers in the clinical cohort.

Investigators noted that the ZUMA-1 and ZUMA-7 cohorts were predominantly of European ancestry, limiting conclusions in non-European populations, and that the number of STXBP2 variant carriers identified was small, warranting confirmation in larger, more diverse cohorts.

Editor’s Note: Leick reports relevant disclosures with BioNTech, Cabaletta Bio, and Adaptimmune.

Leick MB, Sun B, Birocchi F, et al. Genomic correlates of clinical CAR T cell activity. Sci Immunol. 2026;11(121). doi:10.1126/sciimmunol.aef4134

Neelapu SS, Locke FL, Bartlett NL, et al. Axicabtagene ciloleucel CAR T-cell therapy in refractory large B-cell lymphoma. N Engl J Med. 2017;377(26):2531-2544.

Videos

Germline STXBP2 variants may predict severe CAR T cell toxicity, Mark B. Leick, MD, and colleagues find

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Tim Smith joined the MJH Life Sciences team in 2022 and is currently an associate editor for 

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. Previously, he was the producer of the Lungcast podcast. He graduated from UC Berkeley and worked in multimedia journalism as a staff writer prior to joining MJH. You can contact him at tsmith@mjhlifesciences.com.

Upadacitinib (15 mg and 30 mg) met the primary end point of SALT score ≤20 at week 24 in both UP-AA1 and UP-AA2 (P<.001 vs placebo)

The 30-mg dose achieved SALT score ≤20 in 55.0% (UP-AA1) and 54.3% (UP-AA2) of patients, versus 1.5% and 3.4% with placebo

Complete scalp hair regrowth (SALT score 0) was reached by up to 22.5% of upadacitinib-treated patients, a stringent secondary end point

Safety through week 24 was consistent with upadacitinib's other approved indications; no new safety signals were identified

The trials included 118 adolescents (age 12-17 years), broadening the evidence base beyond currently available adolescent options

Two phase 3 replicate randomized clinical trials, UP-AA1 and UP-AA2, found upadacitinib (Rinvoq) significantly outperformed placebo in achieving a Severity of Alopecia Tool (SALT) score of 20 or less at Week 24 in adults and adolescents with severe 

, meeting the primary efficacy end point at both the 15-mg and 30-mg doses.¹

Currently only baricitinib, ritlecitinib, and deuruxolitinib are approved oral JAK inhibitors for severe alopecia areata, and only ritlecitinib carries an adolescent indication, leaving a gap for additional systemic options.¹ Prior trials of these agents left many patients short of the SALT ≤20 threshold, with response rates topping out around 35% across treatment groups.² 

UP-AA1 and UP-AA2 enrolled 1399 patients across 25 and 28 countries, respectively, including 118 adolescents ages 12 to 17 years, making the program one of the largest phase 3 evaluations of a JAK inhibitor in this population.¹

Upadacitinib Efficacy in UP-AA1 and UP-AA2

UP-AA1 and UP-AA2 are global, randomized, double-blind, placebo-controlled phase 3 trials conducted at 112 centers in 25 countries and 125 centers in 28 countries, respectively, from October 2023 to July 2025.¹ Eligible patients were adolescents (age 12-17 years, weight ≥30 kg) or adults (age 18 to <64 years) with a SALT score of 50 or greater and no spontaneous scalp regrowth in the prior 6 months.¹ Patients were randomized 2:2:1 to once-daily 15-mg upadacitinib, 30-mg upadacitinib, or placebo for a 24-week double-blind period, followed by a 28-week blinded extension.¹

Baseline mean SALT score across both trials was 83.9 (SD, 18.9), reflecting a population with extensive scalp hair loss.¹ Both trials met the primary end point: SALT score ≤20 at Week 24 was attained by 45.2% (122/270) of patients on 15-mg upadacitinib and 55.0% (149/271) on 30-mg upadacitinib in UP-AA1, compared with 1.5% (2/135) on placebo (

<.001 for both doses).¹ In UP-AA2, response rates were 44.6% (129/289) with 15 mg and 54.3% (157/289) with 30 mg, versus 3.4% (5/145) with placebo (

Separation from placebo emerged as early as Week 8 for both doses in both trials.¹

Upadacitinib Secondary Endpoints and Safety Profile

Both doses also outperformed placebo on more stringent efficacy measures. Complete scalp hair regrowth, defined as SALT score of 0, was reached by 20.3% of patients on 30-mg upadacitinib in UP-AA1 and 22.5% in UP-AA2, compared with 0% and 0.7% on placebo, respectively (

<.001).¹ Clinician-reported outcomes for eyebrow and eyelash hair loss improved significantly with both doses versus placebo across both trials (

Patients on upadacitinib also reported significantly greater improvement in AA-specific quality-of-life measures, including the Alopecia Areata Symptom Impact Scale and Skindex-16 alopecia areata emotions and functioning domains, at Week 24.¹

Treatment-emergent adverse events (TEAEs) were numerically higher with 30-mg upadacitinib than with 15 mg or placebo, occurring in 67.1%, 62.7%, and 57.1% of patients, respectively, in the pooled safety analysis.¹ The most common TEAEs reported in more than 5% of patients in any group were upper respiratory tract infection, acne, elevated blood creatine phosphokinase, and nasopharyngitis.¹ Serious adverse events occurred in 2.3% of patients on 30-mg upadacitinib, 1.6% on 15 mg, and 0.4% on placebo, with no deaths reported in either trial.¹

Investigators characterized the safety profile as consistent with upadacitinib's other approved indications, with no new safety signals identified.¹

Upadacitinib is already approved for multiple inflammatory indications, including atopic dermatitis, a condition frequently comorbid with alopecia areata.¹ A third study is underway to evaluate long-term efficacy, safety, and dose adjustment strategies through Week 52 of UP-AA1 and UP-AA2, which will help define upadacitinib's place relative to baricitinib, ritlecitinib, and deuruxolitinib in severe alopecia areata.¹

Mostaghimi A, Gooderham MJ, Lynde C, et al. Upadacitinib for severe alopecia areata in adults and adolescents: two phase 3 UP-AA randomized clinical trials. JAMA Dermatol. Published online August 12, 2026. 

King B, Ohyama M, Kwon O, et al; BRAVE-AA Investigators. Two phase 3 trials of baricitinib for alopecia areata. N Engl J Med. 2022;386(18):1687-1699. doi:10.1056/NEJMoa2110343.

Articles

Two large, global phase 3 trials evaluated upadacitinib in adolescents and adults with severe alopecia areata (baseline mean SALT ~84). Both 15 mg and 30 mg once daily achieved robust Week 24 scalp regrowth, with early separation from placebo by Week 8 and meaningful gains across complete regrowth, brows/lashes, and patient-reported quality of life. TEAEs were dose-related and aligned with the known upadacitinib profile; serious events were uncommon and no deaths occurred. Ongoing follow-up will inform durability and positioning versus other oral JAK inhibitors.

In the UP-AA trials, both upadacitinib doses outperformed placebo on SALT score ≤20 at week 24 in adults and adolescents with severe alopecia areata.

Alopecia

UP-AA: Upadacitinib Attains Primary Endpoint in New Alopecia Areata Data

Diana Isaacs, PharmD, is an endocrine clinical pharmacist, director of Education and Training in Diabetes Technology, and codirector of Endocrine Disorders in Pregnancy at the Cleveland Clinic.

Switching patients from daily basal insulin to once-weekly insulin icodec (Awiqli) requires a distinct dosing calculation clinicians have not previously had to apply, given the agent's extended half-life and slower time to steady state. Getting the conversion right matters for glycemic stability during the transition period.

Converting Basal Insulin Patients to Insulin Icodec

, hosts Diana Isaacs, PharmD, and Natalie Bellini, DNP, walked through the practical mechanics of switching patients from existing basal insulin regimens to icodec, the first once-weekly basal insulin approved for type 2 diabetes.

Watch the full episode discussing the commercial availability of Awiqli

The conversion begins with the patient's current total daily basal dose. Rather than simply multiplying by 7 to approximate a weekly equivalent, the initial dose calls for roughly 50% more, reached by multiplying the daily dose by 10.5, because the longer half-life delays time to steady state and a higher starting dose helps patients reach it faster. A patient taking 10 units of daily basal insulin would calculate to approximately 105 units, rounded to the nearest available increment of 100 or 110 units, before returning to a maintenance dose of 7 times the original daily amount, or 70 units weekly, for subsequent doses.

Titration will also depart from familiar basal insulin algorithms. Rather than adjusting every 3-4 days, once-weekly dosing limits adjustment frequency to ≤once per week, with clinicians reviewing 2-4 weeks of fasting and premeal glucose data before making changes, typically in 10% to 20% increments.

Hospital admission poses a separate practical question the hosts addressed directly. Because the average inpatient stay runs <3 days, well short of the weekly dosing interval, clinicians may often leave the icodec regimen untouched during a hospitalization and manage glucose with correction-dose insulin as needed, checking the timing of the patient's last dose. Isaacs and Bellini suggested inpatient glycemic control could ultimately prove more stable under a properly dosed weekly basal regimen, since it is not intended to cover meals or drive overnight drops the way rapid-acting or poorly matched basal doses can.

Patient education needs will differ by starting point. Insulin-naive patients are unlikely to be affected by the larger unit numbers involved, while patients transitioning from daily doses of 10 to 20 units to weekly doses of 70 units or more will need more deliberate counseling to avoid confusion or dosing errors.

Collectively, the hosts framed once-weekly dosing as a meaningful reduction in treatment burden, particularly for patients with caregiver support needs or a history of suboptimal adherence to daily injections, with anticipated gains in patient satisfaction expected to outweigh the learning curve required of both patients and prescribers.

Editors’ Note: Isaacs reports disclosures with Dexcom, Abbott, Lilly, Novo Nordisk, Medtronic, Insulet, and others. Bellini reports disclosures with Abbott Diabetes Care, MannKind, Povention Bio, and others.

Novo Nordisk. Novo Nordisk's Awiqli, the first once-weekly basal insulin for adults with type 2 diabetes, now available in the US. 

. August 11, 2026. Accessed August 12, 2026. 

https://www.prnewswire.com/news-releases/novo-nordisks-awiqli-the-first-once-weekly-basal-insulin-for-adults-with-type-2-diabetes-now-available-in-the-us-302847645.html

In this segment from the latest episode of Diabetes Dialogue, Diana Isaacs, PharmD, and Natalie Bellini, DNP, discuss switching patients from basal insulin to Awiqli.

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Saakshi Khattri, MD, is a board certified Dermatologist, Rheumatologist and Internist and one of only a handful of triple board-certified physicians across the US.

Saakshi Khattri, MD, outlines her key practice-changing takeaways for dermatologists and rheumatologists.

Practice-Changing Perspectives on IL-23 Inhibition and Early Intervention in Psoriatic Disease

In the final segment, Saakshi Khattri, MD, synthesizes practice-changing messages from the risankizumab data across psoriasis and PsA for both dermatologists and rheumatologists.

For dermatologists, she underscores that while no prospective prevention trials have definitively established that any biologic class prevents PsA, retrospective claims and database analyses indicate a class-level signal that IL-23 inhibition may be associated with reduced PsA incidence in patients with psoriasis. On this basis, she considers IL-23 inhibitors, including risankizumab, to be strong systemic options for psoriasis patients, particularly those at elevated risk for joint disease.

From the rheumatology perspective, Khattri points to the 5-year data demonstrating radiographic non-progression and sustained clinical efficacy with risankizumab in PsA as especially important. She notes that the combination of structural protection, durable clinical response, and the agent’s relatively infrequent dosing schedule aligns with key concerns voiced by patients, who often ask about both how long a drug will work and how many injections per year are required. The absence of newly emerging long-term safety concerns further supports its role as a long-term treatment option in appropriate candidates.

Khattri also introduces the concept of a “window of opportunity” in psoriatic disease, drawing an analogy to established paradigms in rheumatoid arthritis. She suggests that earlier initiation of systemic therapy—potentially with IL-23 inhibition, given current data—may offer a chance to influence the trajectory of disease and possibly reduce the likelihood of progression from psoriasis to PsA, even though this remains a hypothesis rather than a proven principle. She concludes by reiterating that, taken together, the data on potential PsA risk reduction, durable radiographic outcomes, and stable long-term safety make IL-23 inhibition, and risankizumab specifically, a valuable component of the therapeutic armamentarium for psoriatic disease.

Video Series

 suggest germline genetic variants may help explain why CAR T cell therapy outcomes vary so widely between patients.

Investigators performed whole genome sequencing on patients with aggressive lymphoma treated with axicabtagene ciloleucel in the ZUMA-1 and ZUMA-7 clinical trials, in partnership with Kite Pharma.

Analysis focused initially on genes associated with hemophagocytic lymphohistiocytosis (HLH), a rare hyperinflammatory syndrome with biochemical similarities to cytokine release syndrome (CRS), the most common toxicity of CAR T cell therapy.

Investigators found that variants in STXBP2 were enriched among patients with high-grade toxicity in the ZUMA-1 cohort, a finding supported by in vitro experiments showing that STXBP2-deficient CAR T cells had impaired degranulation and increased inflammatory cytokine production.

Extending the analysis genome-wide, variants in ADAMTSL3 were linked to protection from toxicity, while variants in PTPN22 were strongly associated with greater CAR T cell expansion, across both ZUMA-1 and ZUMA-7.

HCPLive spoke with Mark B. Leick, MD, a medical oncologist and physician scientist at Massachusetts General Hospital who led the study, about its design and what the findings could mean for CAR T cell manufacturing and patient management going forward.

Q&A: Germline Variants May Predict CAR T Cell Toxicity, With Mark Leick, MD

HCPLive: What motivated you and your colleagues to investigate whether inherited germline genetics could influence outcomes after CAR T cell therapy?

Leick: CAR T cells are different from every other form of therapy that came before. It's not like a Bayer aspirin, where every dose is chemically identical. CAR T cells are manufactured from a patient's own T cells, so they carry all of that patient's ancestral genetic polymorphisms and mutations. Because of this, how CAR T cells behave varies from patient to patient in ways we can't totally understand.

Going into this study, we had some idea of which patients were at high risk of toxicity. Patients with a large tumor burden, or higher baseline levels of inflammation, tend to be more likely to have serious side effects. But beyond that, we didn't have a good understanding of why some patients go through catastrophic toxicities and others don't. It's a little like COVID-19, where some patients end up on a ventilator with severe immune inflammation and others sail through with minimal side effects.

Our hypothesis was founded on a rare disease called hemophagocytic lymphohistiocytosis (HLH), which classically affects pediatric patients, usually kids under age 5. In that disease, patients are born with defects in how their lymphocytes, T cells, and NK cells kill virally infected cells. When those lymphocytes can't kill effectively, they become continually activated and trigger an inflammatory cascade that can become life-threatening.

In the CAR T cell field, we've long recognized that the biochemical features of HLH and CRS after CAR T cell therapy are very similar, and the toxicity mechanism is thought to be similar as well: in HLH it's an inactivated T cell trying to kill a virally infected target, and in CAR T cells it's a CAR T cell trying to kill a tumor target, but the end result is the same, cytokines are produced that activate the myeloid system and drive high fevers, low blood pressure, and other symptoms.

Since HLH has a genetic basis, and we now know less severe forms of these mutations can present later in life, we hypothesized that some of those less severe variants might be present in patients who develop severe toxicity after CAR T cell therapy.

HCPLive: Can you walk our audience through what you eventually found?

Leick: We partnered with Kite Pharma, the largest producer of CAR T cell products, which gave us access to DNA samples, CAR T cell level measurements, clinical data, and serum biochemical data from patients across the ZUMA-1 and ZUMA-7 clinical trials of axicabtagene ciloleucel in patients with aggressive lymphoma.

We performed whole genome sequencing, but because these early CAR T cell trials only included around 100 patients, we needed a narrow hypothesis rather than an unrestricted genome-wide search. So we focused on fewer than 20 genes associated with HLH.

We defined a combined toxicity endpoint that captured patients with high-grade CRS, high-grade neurologic toxicity, or those who received tocilizumab, the antidote for CRS, since those patients likely would have had higher-grade toxicity without it. Among that pool, we found 6 patients with variants in the gene STXBP2, which is involved in lymphocyte degranulation, compared with none in the control cohort without high-grade toxicity.

We followed up with wet lab studies, comparing CAR T cells from patients with the variant to CAR T cells from controls, and found that cells with STXBP2 variants became more inflamed when they encountered target cells. We also introduced the CAR T cell gene and the specific variants into healthy donor T cells and saw the same result in vitro.

We then sought to replicate this finding in the ZUMA-7 cohort, an independent group of patients treated with the same CAR T cell product, but earlier in their line of therapy and with less inflammation overall. We didn't see the same STXBP2 finding there, which we think reflects that these patients had less severe disease and fewer prior treatments.

With both cohorts available, we could also look beyond toxicity. We found that variants in PTPN22 were strongly correlated with CAR T cell proliferation across both ZUMA-1 and ZUMA-7. PTPN22 helps regulate normal T cell biology and serves as a brake on T cell receptor activation, so there's a plausible mechanism: lose the brake, and T cells become more activated and proliferate more.

In fact, 2 patients had the exact same mutation, and that led them to have the highest CAR T cell expansion of all the 100 patients in ZUMA-1, suggesting that there is some sort of gain of function advantage to having that mutation in the context of CAR T.

HCPLive: Is there anything else you'd like to highlight, including any limitations?

Leick: I'd add a couple of limitations. Germline genetics analysis requires comparing genetic variation within populations of comparable ancestry, and because clinical trial accrual in the United States skews toward patients of European ancestry, our study was limited mostly to that population. We only had a couple of non-European patients, not enough to support any meaningful analysis. We'd love to study this in more diverse populations.

Our study was also focused on one product, axicabtagene ciloleucel, so these findings may not apply to other CAR T cell products or disease types beyond lymphoma. We're working in the lab now to understand whether this applies more broadly.

As for clinical implications, this doesn't mean patients with these variants got severely ill. No one died in either trial, and even knowing a patient had these variants, we likely wouldn't manage them differently since we're already fairly good at treating these toxicities. Where I think this becomes more relevant is in choosing donor T cells for allogeneic CAR T cell products, since a single donor's cells can be used to manufacture products for dozens or hundreds of patients, and in using natural human genetic variation as an alternative to CRISPR-based screens to identify genes, like PTPN22, that could be engineered into future CAR T cell products to improve efficacy.

Leick MB, Sun B, Birocchi F, et al. Genomic correlates of clinical CAR T cell activity. 

. 2026;11(121). doi:10.1126/sciimmunol.aef4134

Whole-genome sequencing in aggressive lymphoma treated with axicabtagene ciloleucel implicates germline variation as a contributor to interpatient heterogeneity in CAR T efficacy and toxicity. An HLH-informed candidate approach associated STXBP2 variants with severe CRS/neurologic toxicity in ZUMA-1, supported by in vitro evidence of impaired degranulation and heightened cytokine release. Genome-wide analyses identified ADAMTSL3 variants linked to reduced toxicity and PTPN22 variants correlated with greater CAR T expansion across ZUMA-1 and ZUMA-7. Generalizability is constrained by ancestry and product specificity.

New research links germline genetic variants to CAR T cell toxicity risk and expansion in lymphoma patients treated with axi-cel.

Germline Variants May Predict CAR T Cell Toxicity, With Mark Leick, MD

Robert Sarkany, MD, FRCP, is a consultant dermatologist at St John's Institute of Dermatology at Guy's and St Thomas' Hospital in London and at the Lister Hospital.

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She joined MJH Life Sciences in August 2023 shortly after graduating from Monmouth University where she earned her BA in Communication with a concentration in Public Relations/Journalism and later an MA in Interactive Digital Media. She enjoys traveling, running, and reading books. She can be reached at abrooks@mjhlifesciences.com.

Experts discussed FCS diagnostic scoring tools, diagnostic delays, and new data on olezarsen and plozasiran for lowering triglycerides in a recent clinical forum.

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Victoria Johnson joined MJH Life Sciences in 2020 and has written for NeurologyLive, CGTLive, and is now an assistant managing editor for HCPLive and RheumatologyLive. She doesn’t have enough time for her numerous hobbies. You can reach her at vjohnson@mjhlifesciences.com.

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A Genetic Signature May Predict Who Gets Sick From CAR T Cell Therapy

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