The recent discovery of somatic splicesomal mutations in MDS has revealed a new leukemogenic pathway involving spliceosomal dysfunction.2, 3 Somatic mutations in the splicing factor genes SF3B1, U2AF1, SRSF2 and ZRSR2 are frequent in MDS patients.4 Importantly, these genes encode proteins that are all involved in 3′-splice site recognition during pre-messenger RNA (pre-mRNA) processing. This evidence concerns the gene SF3B1 and myelodysplastic syndrome.