These findings would align with the idea that cancer cells harboring heterozygous mutations in SF3B1 (or in other splicing factors such as SRSF2 or U2AF1) are dependent on their WT allele for splicing function and cell survival (Zhou et al, 2015; Fei et al, 2016; Lee et al, 2016) and are therefore more sensitive to splicing inhibitors. Here, SRSF2 is linked to cancer.