Different responses to ICB may be attributed to several factors that directly or indirectly affect cytotoxic T lymphocyte (CTL) recruitment and activation, including the tumor mutational burden, expression of programmed cell death protein 1 (PD-1) and programmed death ligand 1 (PD-L1), homologous repair deficient and proficient phenotypes, and the tumor microenvironment (Tregs, M2-type tumor-associated macrophages (TAMs), plasmacytoid DCs, N2-type neutrophils, and myeloid-derived suppressor cells (MDSCs)) [4, 5]. This evidence concerns the gene PDCD1 and neoplasm.