1). We therefore observed a more variable fadraciclib response with KMT2A-PTD status not being a predictor for better treatment response. This is consistent with previous results showing that the CDK9-specific inhibitor atuveciclib inhibits the proliferation of seven AML cell lines, regardless of KMT2A-r status64. In addition, atuveciclib displayed potent in vitro activity in 80% of AML patient samples harboring KMT2A WT, including those with mutant NPM1 or FLT3-ITD. This evidence concerns the gene CDK9 and acute myeloid leukemia.