These data were also recapitulated in AML patients carrying FLT3-ITD mutation, where the treatment with the FLT3 inhibitor AC220 induced the BRCAness phenotype in FLT3-ITD-mutated cells, with downregulation of HR and NHEJ proteins including BRCA1, BRCA2, PALB2, RAD51, and LIG4 and enhanced sensitivity to talazoparib and olaparib [136]. The gene discussed is PALB2; the disease is acute myeloid leukemia.