More than 20% of AML patients have defects in chromosome segregation, also supported by an altered activity of the SAC components, caused by BUB1 deregulation, BUBR1 repression, or aberrant expression of MAD2 and CDC20 [9, 144, 145], that was further exacerbated by decitabine treatment in AML cell lines [144]. This evidence concerns the gene BUB1 and acute myeloid leukemia.