Given the short half-life of the rat anti-mouse PD-L1 antibody that was used here, it is suggested that the beneficial effect of the immunotherapy for AD and dementia does not require continuous exposure to the antibody, and that the effect is mechanistically different from that underlying the current anti-PD-L1 treatment used in cancer therapy79,80; it is therefore expected to have minimal adverse immunological effects. The gene discussed is CD274; the disease is cancer.