As deactivating TP53 mutations can be found in ~10% of AML cases [31], these mutations would enable TP53 mutant clones to decrease their dependence on OXPHOS, upregulation of which is essential for HSC differentiation, allowing cells to remain in an undifferentiated state, enabling disease establishment and progression, while also making them reliant on pyruvate stores [230]. Here, TP53 is linked to acute myeloid leukemia.