Like EZH2, PRC1 functions in AML to regulate bivalent loci and keep key differentiation genes silenced, which contributes to the maintenance of PRC2 repression at these loci as well.88 This has provided the rationale for inhibition of PRC1 to differentiate leukemic cells, with varying levels of success, as discussed below. Here, EZH2 is linked to acute myeloid leukemia.