For example, the formation of complexes between the MLL-binding pocket of WDR5-MLL and the p30 isoform of C/EBPα represents a functional vulnerability that can be pharmacologically exploited by the small-molecule antagonist OICR-9429 to trigger differentiation and growth arrest in C/EBPα-mutant AML.154 Drug resistance and limited therapeutic efficacy are key issues that hinder the clinical application of cofactor inhibitors. Here, CEBPA is linked to acute myeloid leukemia.