In the second step, mAbs induce a long‐term cytotoxic T‐cell response against the tumor.[18, 19, 20] In a model of FcγR‐humanized mice it has been demonstrated that the rapid ADCC against tumor cells requires hFcγRIIA activation on macrophages, while the long‐term anti‐tumor cytotoxic T cell response requires hFcγRIIA‐mediated cross‐presentation.[21] In addition, CD47‐SIRPα inhibition triggers the efficient uptake of cell‐associated antigens in type 2 DCs.[22]. This evidence concerns the gene FCGR2A and neoplasm.