By accelerating STAT3 phosphorylation and increasing NOTCH-1 signaling, loss-of-function variants in SH2B3 have been linked to the oncogenesis of myeloproliferative neoplasms (MPN), early T-ALL, Ph-like ALL, B-ALL, and non-malignant hematological disorders [141,142,143,144]. The gene discussed is STAT3; the disease is myeloproliferative disorder.