SF3B1 and myelodysplastic syndrome: This would be consistent with the recruitment of U2-small nuclear ribonucleoprotein to positions 5′ of the BP in response to SF3B1 targeting drugs.47 Emerging data suggest that myeloid malignancies with splicing factor gene mutations are preferentially susceptible to additional splicing perturbations induced by splicing factor inhibitors48 and this may also represent a therapeutic approach in SF3B1-mutant MDS.