CEBPA and acute myeloid leukemia: These include (but are not limited to) acquired biallelic mutations in CEBPA (41, 42) which lead to differentiation blocks in some AML subtypes (38), NRAS, ASXL1, SETBP1, NPM1, and WT1 secondary mutations (43), chromosomal abnormalities (monosomy 7 or trisomy 8) (44)), disrupting the regeneration abilities of enhancers (45), HSC exhaustion following repeated infections, and changes in DNA binding affinities that result in disruptions to interaction partners/target genes.