Compounds might actdirectly on T-cells by enhancing anti-tumor cytokine pathways (e.g., IFNg,TNFa), agonizing cytolytic pathways, or enhancing perforin or cytolytic granzymesynthesis/secretion (Fig. 1a: 1 and 2).Alternatively, compounds might act via tumor cells to affect T-cell killing; byincreasing MHC class I expression and/or antigen processing/presentation orupregulation of co-stimulatory molecules (Fig. 1a: 3). This evidence concerns the gene TNF and neoplasm.