In anti-PD-1–treated cohorts, responders with NSCLC display higher circulating acetate, propionate and butyrate; mechanistically, butyrate increases H3K27ac at PDCD1 and CD28 regulatory regions, augmenting TCR signaling and cytotoxicity, thereby potentiating anti-PD-1 therapy [92]. This evidence concerns the gene PDCD1 and non-small cell lung carcinoma.