While most of these antagonist receptors behave as decoy receptors when co-expressed with agonist receptors on the cell surface or within the tumor microenvironment [15], DcR2 has, in addition, been found to be able to interact directly with both DR4 and DR5, restraining caspase-8 recruitment and activation [16,17]. This evidence concerns the gene TNFRSF10A and neoplasm.