In murine melanoma and colon cancer models, pharmacologic or genetic inhibition of the writer METTL3 enhanced tumor control by sustaining CD8+ T-cell cytotoxicity and reducing exhaustion-associated features, thereby improving responses to anti-PD-1; single-cell RNA-seq also showed expansion of activated, less-exhausted CD8+ states under METTL3 inhibition (85). This evidence concerns the gene CD8A and melanoma.