As previously hypothesized, the soluble forms of PD-1 and PD-L1 may retain a binding ability similar to their membrane-bound counterparts as well as the capacity to exert significant biological actions; sPD-L1 may bind to sPD-1 on T cells, thus disrupting their activation and enhancing the immune escape of tumor cells, while, in contrast, sPD-1 may bind to and potentially inhibit membranous-bound PD-L1, thus leading to restoration of the antitumor T-cell function [36,40,41]. This evidence concerns the gene PDCD1 and neoplasm.