[1,5,6,28] By binding to co-factors, C-terminal mutated C/EBPα proteins can sequester these proteins away from chromatin, thereby functioning in a dominant-negative manner.[5] AML patients frequently harbor an N-terminal frameshift mutation on one allele together with a C-terminal mutation on the other one, resulting in biallelic expression of different CEBPA mutants. Here, CEBPA is linked to acute myeloid leukemia.