Loss-of-function mutations in SH2B3 are reported to play an important role in the oncogenesis of myeloproliferative neoplasms (MPN), early T-ALL, Ph-like ALL, B-ALL and nonmalignant hematological diseases by accelerating STAT3 phosphorylation and increased NOTCH-1 signaling [130,131,132,133]. Here, STAT3 is linked to myeloproliferative disorder.