Due to the strong impact of DOT1L inhibition on proliferative signaling and the induction of myeloid differentiation irrespective of MLL-r, we hypothesized that treating both MLL-r and non-MLL-r AML cells with Pinometostat would induce sensitization to further treatment with the multi-kinase inhibitor Sorafenib. The gene discussed is KMT2A; the disease is acute myeloid leukemia.