These drugs modify the immune microenvironment via several mechanisms, including better immunogenicity induced by tumor apoptosis [25], [26], upregulations of tumor-associated antigens and mannose-6-phosphate (M6P) expressions and modulation of Fas/TRAIL-dependent pathway sensitize tumor cells to cytotoxic T lymphocytes (CTLs) [27]–[29], elimination of Tregs [30], [31], and disruption of tumor stromal caused larger numbers of tumor-infiltrating CTLs [32]. The gene discussed is TNFSF10; the disease is neoplasm.