Physiologically, binding of PD-L1 to its receptor program death 1 (PD-1) on T cells constitutes a “safety brake” to prevent over-reactive host immunity, whereas, pathologically, in cancer cells, aberrant expression of PD-L1 and its binding to cytotoxic T cells act as a “stop sign” to counter the proliferation and function of T cells, thus augmenting the tumor evasion of host anti-tumor immunity. This evidence concerns the gene PDCD1 and cancer.