Although U2AF1MUT does not generate widespread splicing alterations, altered splicing events driven by U2AF1MUT belong to mutated genes in MDS and AML (ASXL1, GNAS, PICALM) and involved in cancer hallmarks, including stem cell biology (MED24), transcription regulation (H2AFY), replication stress response pathway (ATR), and innate immune pathway (IRAK4) [16,20,54,59]. This evidence concerns the gene IRAK4 and acute myeloid leukemia.