Somatic STAT3 GOF mutations have been identified as key driver mutations in T cell large granular lymphocytic leukemia (T-LGLL) and chronic NK lymphoproliferative disease (CLPD-NK), and STAT5B GOF mutations are also present in both T-LGLL and CLPD-NK at a lower frequency [42], as well as other T cell neoplasms [90] and myeloid neoplasm with eosinophilia and hypereosinophil syndrome (HES)/early onset eosinophilia [91,92], and has also been observed in chronic neutrophilic leukemia [93]. Here, STAT3 is linked to hypereosinophilic syndrome.