The corresponding mutation in STAT5B was subsequently identified as a somatically acquired driver mutation in 1–37% of patients with various lymphoid neoplasms including large granular lymphocytic leukemia [16], paediatric T-cell acute lymphoblastic leukemia [28], T-cell prolymphocytic leukemia [29], γδ-T-cell lymphoma [30] and two cases of lymphocyte-driven early onset nonclonal eosinophilia with urticaria, dermatitis and other features [17]. The gene discussed is STAT5B; the disease is T-cell prolymphocytic leukemia.