Interestingly, STAT3 and STAT5 mutations in hematopoietic cancers exist in a mutually exclusive manner and often co-occur with mutations in DNA-modifying enzymes such as DNA methyltransferase 1/3A (DNMT1/3A), Ten-eleven translocation methylcytosine dioxygenase 1/2 (TET1/2), or isocitrate dehydrogenase 2 (IDH2), and corepressor molecules with histone deacetylase (HDAC) activity such as BCL6 Corepressor (BCoR)/Nuclear receptor corepressor 1/2 (NCoR1/2) [16]. This evidence concerns the gene STAT5A and hematopoietic and lymphoid cell neoplasm.