The deficiency in PRMT5 leads to changes in ASE among several crucial genes, the normal function of which is vital for AML cell survival.290 A comprehensive CRISPR/Cas9 domain screen targeting 490 classical RBPs uncovered the RBP dependence in human cancers.291 Importantly, RBM39 can inhibit cassette exon inclusion and promote intron retention in mRNAs encoding HOXA9 and other RBPs preferred by AML. Here, PRMT5 is linked to acute myeloid leukemia.