Figure 4 depicts the mechanism of PD-1/PD-L1 ICB and T-cell activation. A binding interaction between PD-1 and its primary ligand, PD-L1, results in the inhibition of T cell activation, cytokine release and cytotoxicity. Additionally, this interaction induces exhaustion and apoptosis of tumor-specific T cells; therefore, it regulates immunological responses and enables tumor cells to evade immune surveillance [73]. In a recent study, PD-L1 expression was more prevalent in liver and lung metastatic foci compared to the primary tumor [74]. This evidence concerns the gene CD274 and neoplasm.