Studies showed that the exhaustion of antigen-specific T cells caused by one pathogen or cancer could lead to exhaustion of other antigen-specific T cells through nonspecific pathways, such as the high-level co-expression of multiple inhibitory receptors like PD-1(CD279), cytotoxic T lymphocyte antigen-4 (CTLA-4, CD152), and lymphocyte-activation gene 3 (LAG3), which bring more severe repercussions [30, 32]. The gene discussed is LAG3; the disease is cancer.