inhibition of BTK downregulates expression of myriad downstream signaling molecules, most prominently PLCγ2, some mutations in which seem to mediate ibrutinib resistance. Interestingly, a clinically similar eruption-a lymphohistiocytic infiltrate with eosinophils responsive to corticosteroids-has been described in patients with mutations in the PLCγ2 gene. 6 In conclusion, treatment of lymphoid leukemias with the BTK inhibitor ibrutinib can lead to development of a panniculitis, which may be induced by drug-induced immune modulation. Previously uncharacterized, this painful rash typically occurs early during drug exposure and responds well to systemic corticosteroid use; however, low-dose maintenance therapy may be necessary to prevent recurrence.