SRSF2 and myelodysplastic syndrome: In these cases, RBM39 can interact with SF3B1 and U2AF65, targeting HOXA9 and thus promoting intron retention.282 Another review has concluded that SRSF2 is mutated in more than 20% of MDS and 50% of chronic myeloid leukemia, causing expansion of the hematopoietic progenitor cell lineage, increased proliferation, apoptosis, and peripheral hematopoiesis.283 However, such comprehensive reviews are limited to other hematological tumors.