In addition, knockdown of KMT2A and treatment with Mi-503, a small molecule inhibitor of the KMT2A-MEN1 axis, resulted in decreased H3K4me1 promoter occupancy and decreased expression of PLK1. While translocations and PTD of KMT2A have long been implicated in AML pathogenesis, <1% of CMML patients demonstrate KMT2A translocations22 and no patients had KMT2A PTD in our study. This evidence concerns the gene MEN1 and chronic myelomonocytic leukemia.