By contrast, the p53 R248W mutant promotes hematopoietic stem cell (HSC) self-renewal through its GOF interaction with EZH2 (19), whereas the p53 R172H mutant (corresponding to human R175H) exhibits GOF activity in AML via activation of the embryonic transcription factor (TF) Foxh1 (20). The gene discussed is TF; the disease is acute myeloid leukemia.