To achieve tumour‐localised CD40 stimulation without systemic FcγR crosslinking, we designed CD40‒HER2 BsAbs with an N297A Fc mutation, which eliminates FcγR binding to prevent antibody‐dependent cellular cytotoxicity against CD40‐positive APCs and HER2‐independent CD40 activation (Figure 1A).7, 8, 9. The gene discussed is CD40; the disease is neoplasm.