Given that the misregulation of H3K4 methylation resulting from MLL fusion proteins, mutant MLL3 and MLL4 proteins, and aberrant demethylase activity has been implicated in cancer progression27, 28, 29, our observations linking the H3K4 regulator SETD1A in tumorigenesis supports the importance of this chromatin modifier and the potential application of small molecules targeting the enzymatic activity of KMTs in cancer. The gene discussed is KMT2A; the disease is cancer.