To decipher how transcriptional reprogramming driven by SF3B1 mutation affected erythroid lineage, we expanded erythroblasts from CD34+ hematopoietic stem and progenitor cells (HSPCs) collected from 14 SF3B1MUT, 10 without SF (SF3B1, SRSF2, U2AF1) mutation (SFWT) MDS and 6 healthy controls (Fig. 2a). This evidence concerns the gene SRSF2 and myelodysplastic syndrome.