Although the mechanism of the enhancement sensitivity to splicing inhibitors is unknown, probably because a mutated SF3B1 gene may be unable to tolerate further perturbations in splicing and therefore be preferentially sensitive to pharmacological splicing inhibition [134], these findings suggest that there may be a therapeutic window for the use of spliceosome modulators in the treatment of hematologic malignancies with SF3B1 mutation [85]. Here, SF3B1 is linked to hematologic disorder.