The tumor microenvironment is resulted from the presence of immune checkpoint inhibitors, such as programmed death-1/programmed cell death ligand (PD-L1), cluster of differentiation 47 (CD47), T cell immunoglobulin and mucin-containing domain-3 (TIM3), lymphocyte activation gene 3 (LAG3) and cytotoxic T-lymphocyte antigen-4 (CTLA4) [8–10]. This evidence concerns the gene HAVCR2 and neoplasm.