First, since UTX is a H3K27 demethylase, several research groups have shown that inhibitors of EZH2, the H3K27 methyltransferase, can strongly inhibit the growth of UTX-deficient cancers.6,9 Second, in pancreatic cancer models it was found that UTX-deficient cancer is sensitive to BET inhibitors, which restrain gene expression from super-enhancers that are altered by UTX loss.4 Third, two separate studies suggest that the cellular sensitivity to cytarabine, a cytosine analog that inhibits DNA synthesis, is potentially affected by the H3K27 methylation status. This evidence concerns the gene KDM6A and familial pancreatic carcinoma.