The clinical response to ICB has been shown to correlate with (1) the mutational load (non-synonymous/frameshift mutations) of tumors, presumably associated with the expression of neoantigens; (2) expression of PD-L1 by tumor cells (cell membrane-associated ligand of the PD-1 checkpoint receptor); and (3) the abundance of circulating Ki67+CD8+ T cells relative to the tumor burden. The gene discussed is CD274; the disease is neoplasm.