Since tumor cell–intrinsic PRC2 loss drives an immune-desert TME, we speculated that PRC2 loss might confer primary resistance to FDA-approved ICB immunotherapies, including anti–programmed cell death 1 (anti–PD-1) and anti–cytotoxic T lymphocyte–associated protein 4 (anti-CTLA4) antibodies (48). This evidence concerns the gene CTLA4 and neoplasm.