Specifically, AML development in this model is driven by the homozygous expression of the CebpaLp30 allele thereby phenocopying bi-allelic CEBPA mutant AML (affecting 7–10% of AML patients) where the truncated CEBPA-p30 variant constitutes the sole functional CEBPA isoform [8, 9]. Here, CEBPA is linked to acute myeloid leukemia.