Immune escape and tolerance in the tumor microenvironment are closely involved in tumor progression, caused by T cell exhaustion, and mediated by inhibitory signals based on the activation of immune-checkpoint molecules, including programmed death-1 (PD-L1), cytotoxic T lymphocyte-associated protein 4, and T cell immunoglobulin and mucin domain-containing-3 (TIM-3)14–16. This evidence concerns the gene HAVCR2 and neoplasm.