In the AML, studies have revealed that PARP1 is overexpressed in the AML with FMS-related receptor tyrosine kinase 3 internal tandem duplications (FLT3-ITD) mutation, driving PARylation of STAT5 to sustain partial STAT5 signaling activation and promote AML survival and proliferation [7]. This evidence concerns the gene PARP1 and acute myeloid leukemia.