Beyond m6A, A-to-I editing by ADAR1 in macrophages functions as an immune brake: macrophage-specific Adar1 loss, especially when combined with IFN-γ, induced tumor regression across melanoma, lung, and colon cancer models via heightened antiviral-like signaling (PKR/eIF2α) and cytokine remodeling (94). This evidence concerns the gene ADAR and colonic neoplasm.