Major histocompatibility complex class I (MHC-I) gene promoters are bivalently modified during development, which can be exploited in cancer cells to silence MHC-I expression and evade CD8+ T cells; in cells that exhibit bivalent modification of MHC-I genes, lower levels of cell surface MHC-I can be induced either by PRC2 inhibition or exposing the cells to interferon γ (IFNγ) in conjunction with polycomb inhibition to allow a permissive chromatin status.