Tumor-intrinsic studies provide convergent, mechanistic evidence that the m6A reader YTHDF1 curtails antigen visibility: loss of YTHDF1 in cancer cells limits the translation of lysosomal genes, reduces lysosomal proteolysis of MHC-I and tumor antigens, upregulates surface MHC-I, and converts immunologically “cold” tumors into “hot” ones that respond to checkpoint blockade; notably, anti–PD-L1 or anti–CTLA-4 co-therapy is markedly more effective when YTHDF1 is disrupted, underscoring a causal link between m6A-readout and antigen presentation–driven immunity. Here, CTLA4 is linked to neoplasm.