In addition, we show (i) that the heterozygous disruption of the bZIP domain in a wt background leads to an impediment of granulocyte differentiation, but does not confer self-renewal capacity (ii) that the primary mutational pattern (SRFS2 and RUNX1) leads to dysplasia of erythroid and myeloid lineages, and (iii) that the additional introduction of the CEBPA mutation causing the disruption of the bZIP domain leads to a combination of both, and promotes self-renewal capacity of HPCs, thus mimicking the increased risk of AML development seen in the patient. Here, RUNX1 is linked to acute myeloid leukemia.