Recurrent somatic mutations in a subset of spliceosome genes (SF3B1, SRSF2, and U2AF1) are frequently identified (30–60% depending on disease phenotype) in patients afflicted with myelodysplastic syndromes (MDS), myeloproliferative neoplasms (MPN) such as myelofibrosis (MF), MDS/MPN overlap disorders such as chronic myelomonocytic leukemia (CMML), and secondary acute myeloid leukemia (sAML).1-8 These heterozygous and mutually exclusive mutations are enriched in hotspot codons in these 3’ splicing factor proteins resulting in aberrant alternative mRNA splicing in hematopoietic cells. This evidence concerns the gene SF3B1 and myelodysplastic syndrome.