Multiple mechanisms have been proposed including augmentation of inflammation and immune infiltration tumor microenvironment (e.g. making tumors “hot”) (11, 13, 16), enhanced cytokine signaling mediating CD8+ T-cell and NK cell dependent cytotoxicity (10, 14), and alteration of the gut microbiome promoting accumulation of metabolites that augment the efficacy of ICI via CD8+ T cells (15). Here, CD8A is linked to neoplasm.