Tumor-intrinsic loss of the m6A reader YTHDF1 converts “immune-desert” lesions into T cell–inflamed tumors by curbing lysosomal translation, stabilizing MHC-I on the surface, and enhancing antigen persistence; these changes coincide with broader remodeling of the tumor microenvironment (TME) with increased CD8+ T-cell infiltration and improved checkpoint response in mouse models. The gene discussed is YTHDF1; the disease is neoplasm.