Across a range of tumor types we find that PRC2 silences critical genes essential for MHC-I antigen processing, leading to upregulation of multiple MHC-I APP genes following PRC2 inhibition, including those encoding an MHC-I transactivator (NLRC5), immunoproteasome components (PSMB8 and PSMB9), peptide transporters associated with antigen processing (TAP1 and TAP2), and MHC-I heavy chains (HLA-B and HLA-C) (Figures 2I and S2D). This evidence concerns the gene APP and neoplasm.