Provided the reported prevalence and driving role of STAT3 mutations7 in CLPD-NK and the previous findings of mutations of the STAT protein interactor FLT3 in a T-LGLL patient without STAT lesions3, we searched for mutations in genes functionally related to JAK/STAT signaling in CLPD-NK patients, starting from STAT3 and STAT5B interactors in STRING database: only PTK2/FAK1 was mutated in patient #1253 (VAF 0.35), as previously reported3. Here, SOAT1 is linked to T-cell large granular lymphocyte leukemia.