Unlike previously described mechanisms of tumor cell–intrinsic immune evasion that primarily affect selective subpopulations of tumor immune infiltrates by, for example, decreasing T lymphocyte infiltration and function or recruiting myeloid-suppressive cells (e.g., LKB1 mutation in lung cancer) (47, 51–59), our study showed that PRC2 loss in tumors affected a broad spectrum of subpopulations of immune infiltrates, including DCs, T cells, B cells, and/or macrophages, and therefore drives an immune-desert TME, consistent with a prior proteomics study of MPNST (60). This evidence concerns the gene STK11 and neoplasm.