Hence, while clinical implications of the STAT5B mutations are still ambiguous and are likely to be not strong enough to define the disease course, we confirmed in Tγδ LGLL, as previously reported in Tαβ LGLL18, that STAT3 mutations characterize neutropenic patients, supporting the hypothesis we recently proposed that the activation of STAT3 accounts for the molecular mechanisms, related to the miR-146b/Fas ligand axis46, that ultimately lead to neutropenia. The gene discussed is FASLG; the disease is neutropenia.