Surprisingly, hematopoietic differentiation of these AML-iPSCs and leukemia formation was sufficient to reestablish the leukemic DNA methylation and gene expression profile strongly suggesting that the genetic mutations/rearrangements of the KMT2A/MLL locus in AML-iPSCs reactivate a leukemic program in the context of hematopoietic cells (41). This evidence concerns the gene KMT2A and acute myeloid leukemia.