Overexpression of inhibitory receptors, including programmed cell death protein-1 (PD-1), cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and T cell immunoglobulin mucin 3 (TIM-3), on T cells of cancer patients has been shown to counteract with co-stimulatory cell signals, leading to progressive loss of their activation potential and effector functions, exhaustion and eventually deletion [107,108,109]. The gene discussed is HAVCR2; the disease is cancer.