Our results also show that introducing a CEBPA mutation disrupting the bZIP domain on the background of additional mutations (RUNX1 and SRSF2) but not by itself increased the self-renewal capacity of the committed progenitor cells and blocked myeloid differentiation, which is the main characteristic of high-risk MDS and AML. The gene discussed is SRSF2; the disease is myelodysplastic syndrome.