Cutaneous T-cell lymphomas (CTCLs) are a group of lymphoid neoplasms with high relapse rates and no curative treatment other than allogeneic stem cell transplantation (allo-SCT). CTCL is significantly influenced by disruption of JAK/STAT signaling. Therefore, Janus kinase (JAK) inhibitors may be promising for CTCL treatment. This study is a systematic review aiming to investigate the role of JAK inhibitors in the treatment of CTCL, including their efficacy and safety. Out of 438 initially searched articles, we present 13 eligible ones. The overall response rate (ORR) in the treatment with JAK inhibitors in clinical trials was 11–35%, although different subtypes of CTCL showed different ORRs. Mycosis fungoides showed an ORR of 14–45%, while subcutaneous-panniculitis-like T-cell lymphoma (SPTCL) displayed an ORR ranging from 75% to 100%. Five cases were reported having a relapse/incident of CTCL after using JAK inhibitors; of these, three cases were de novo CTCLs in patients under treatment with a JAK inhibitor due to refractory arthritis, and two cases were relapsed disease after graft-versus-host disease treatment following allo-SCT. In conclusion, using JAK inhibitors for CTCL treatment seems promising with acceptable side effects, especially in patients with SPTCL. Some biomarkers, like pS6, showed an association with better responses. Caution should be taken when treating patients with an underlying autoimmune disease and prior immunosuppression.

Neutrophilic dermatoses, including pyoderma gangrenosum (PG) and Sweet syndrome (SS), are inflammatory disorders characterized by neutrophilic infiltration without infection. Conventional therapies are often inadequate. We aim to evaluate the efficacy and safety of JAK inhibitors (JAK‐I) in the treatment of PG and SS. The study was registered (PROSPERO‐CRD420251113331), and a relevant search was conducted on PubMed/MEDLINE, Scopus, Web of Science, and Embase until July 27, 2025. Included studies were English language reports describing PG or SS treated with any JAK‐I or cases of JAK‐I–associated SS. Reviews, animal studies, and reports with insufficient clinical data were excluded. Four reviewers independently screened records. Data extraction included demographics, comorbidities, treatment regimens, outcomes, and adverse events. Risk of bias was assessed using the National Heart, Lung, and Blood Institute and Murad et al. tools through discussion‐based consensus. Due to heterogeneous outcome definitions and small sample sizes, only descriptive synthesis was performed. Fifty‐four reports, including 70 patients (59 PG, 5 SS) treated with JAK‐I and 6 JAK‐I–associated SS, were included. Across 43 PG studies, five JAK‐Is—tofacitinib, upadacitinib, baricitinib, abrocitinib, and ruxolitinib—produced 33 complete and 26 partial responses. Twenty‐six patients (44.1%) received monotherapy. Most patients (51/59; 86.4%) had at least one comorbidity. Adverse events occurred in 6 (10.1%), including anemia, hypertension, renal dysfunction, fatigue, and acneiform eruption. Among 11 SS reports, all 5 treated patients achieved complete resolution with baricitinib, ruxolitinib, or filgotinib. Six additional cases described ruxolitinib‐associated SS, generally improving with corticosteroids or drug withdrawal. Most studies were rated good quality. Evidence is limited to small cases with heterogeneous outcome definitions, variable dosing, and inconsistent follow‐up. JAK‐Is are associated with clinical improvement in PG and selected SS cases and may serve as useful adjunct therapies, though caution is needed in patients with hematologic malignancies. Larger controlled studies are needed.

Background: Mycosis fungoides (MF) is a type of cutaneous T‐cell lymphoma (CTCL) with slow progression, usually presenting with patches and plaques. The infiltration of histiocytes and eosinophils in skin cancers can mask the underlying condition, posing a diagnostic challenge. While cases of MF associated with tissue eosinophilia or histiocytosis infiltration resembling Langerhans cell histiocytosis (LCH) have been reported, the simultaneous occurrence of both conditions in a single MF patient has not been documented. Case: In this case report, we presented an elderly man with a known history of patch and plaque‐stage MF who developed a large cutaneous tumor on his right mandibular margin. Multiple biopsies initially led to misdiagnoses, attributing the lesion to Well's syndrome and LCH due to the dense infiltration of eosinophils and histiocytes, respectively. However, the absence of a BRAF V600 mutation and lack of clinical correlation reduced the likelihood of these initial diagnoses. After repeated biopsies and a thorough evaluation by hematopathology and dermatopathology specialists, the findings were reassessed, leading to the consideration of tumoral MF with reactive eosinophil and histiocyte infiltrates. The patient was subsequently started on chemotherapy and phototherapy, which led to tumor regression after treatment initiation. Conclusion: This case highlights the importance of considering MF in patients presenting with tissue eosinophilia or Langerhans cell infiltration, even when initial biopsies lack definitive features.