On the other hand, a PRMT1 inhibitor, AMI-408 could also significantly extend disease latency and OS in mouse models carrying MLL-GAS7 fusion or MOZ-TIF2.42 Similarly to DOT1L inhibitors, the efficacy of PRMT1 inhibitors in leukaemia suppression was far inferior to those by genetic or shRNA approaches, indicating the need to improve the pharmacokinetics of these early phase inhibitors. This evidence concerns the gene KMT2A and leukemia.