These drugs can modulate the immunogenicity of tumor cells through different mechanisms including (1) increasing the expression of tumor antigens and enhancing tumor antigen presentation; (2) upregulating costimulatory molecules (B7-1) and downregulating coinhibitory molecules (B7-H1/PDL1) expressed on the tumor cell surface, which in turn increases effector T-cell function; (3) increasing T-cell mediated lysis of tumor cells through granzyme and perforin-dependent mechanisms; and (4) reducing the infiltration of MDSCs and Tregs in the tumor microenvironment (Figure 2). Here, PRF1 is linked to neoplasm.