As this activation is unlikely to be mediated by enavatuzumab through mouse TweakR on the immune cells, the function of enavatuzumab on mouse immune effector cells is likely through Fc-FcγR ligation; such “bridging” between the FcγR on immune cells and TweakR on the tumor target cells, as suggested in the PBMC-tumor cell co-culture studies, is probably required for triggering effector cell activation in vivo. This evidence concerns the gene TNFRSF12A and neoplasm.