We have previously identified an evolutionarily conserved synthetic lethality between loss of SETD2 and WEE1 inactivation, and that renal tumours with loss of SETD2 or H3K36me3 can be specifically targeted with WEE1 inhibition, an observation that has been taken into clinical trials [24, 73, 74]. This evidence concerns the gene WEE1 and kidney neoplasm.