In a study of mutational status of three SF genes (SF3B1, U2AF1 and SRSF2), NPM1, FLT3, CEBPA, IDH1, DNMT3A, ASXL1 and NRAS/KRAS in 344 patients, including 47 refractory anemia with excess blasts (RAEB), 29 AML with low BM blast count and other AML patients, Taskesen et al could not find any molecular association.[10] However, with the help of combined genome-wide mRNA expression and DNA-methylation profiling they identified two distinct patient clusters highly enriched for SF-mutated RAEB/AML. This evidence concerns the gene NRAS and myelodysplastic syndrome with excess blasts.