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. Here, SF3B1 is linked to myelodysplastic syndrome.