Mutations of U2AF1 have been implicated in MDS patients with MDS disease without an increase in ring sideroblasts (MDS without RS), chronic myelomonocytic leukaemia, de novo AML and myeloproliferative neoplasms.21 U2AF1‐S34F impaired erythroid differentiation and reduced growth of erythroid progenitors in human haematopoietic progenitors. This evidence concerns the gene U2AF1 and chronic myelomonocytic leukemia.