As seen in previous publications in T‐ALL murine xenograft models, the patient showed a remarkable response of the skin lesions with ruxolitinib, independently of the presence of JAK1 or JAK2 mutations.14 Inline, JAK3 M511I was found to obtain an increased JAK/STAT signaling by acquiring an additional mutation in the pseudokinase domain, which was also present in our patient.15 This evidence concerns the gene SOAT1 and acute lymphoblastic leukemia.