These results suggest that the novel mAbs directly affect the CTLA-4 function on tumor cells by inhibiting the downstream survival pathways, such as that of PI3K, and by inducing apoptosis in a similar fashion to CD-80 and CD-86 ligands, that induced apoptosis by caspase 3 activation, as also previously reported in literature [15,16,18]. The gene discussed is CD86; the disease is neoplasm.