By deriving Leukemia-iPSCs (LiPSCs) genetically matched but epigenetically distinct from the parental cell lines, the authors showed that: (1) genetic and epigenetic alterations are both required to maintain the leukemic potential; (2) BCR-ABL fusion protein is able to trigger DNA methylation changes that contribute to leukemia formation and (3) nuclear reprogramming can erase aberrant DNA methylation, thereby delaying the onset of the malignancy. This evidence concerns the gene ABL1 and leukemia.