In conclusion, although evidence from early studies (21, 25) suggested that MLL-SEPT fusion formation was likely due to this hypothesis that exposure to drugs targeting topoisomerase II can result in double-strand DNA breaks that trigger the error-prone non-homologous end joining pathway, the molecular mechanism that whether MLL-SEPT5 fusion can induce the transformation of MDS to AML require further investigations through experiments. The gene discussed is KMT2A; the disease is acute myeloid leukemia.