Moreover, small-molecule compounds that target the essential splice factor SF3B, such as spliceostatin A and E710758,59, have shown efficacy in leukemia models harboring mutations in the same or different trans-acting splice factors, namely SF3B1, SRSF2, or U2AF35, which sensitize the cells to the inhibitors60–63, though inhibition of SF3B also evokes global intron retention and cytotoxicity. This evidence concerns the gene U2AF1 and leukemia.