In the present study, using Aβ42‐treated MdM and d‐THP‐1 cells as in vitro models of microglia in AD, MaR1 was shown to have protective effects, including reduced secretion of pro‐inflammatory cytokines and chemokines, improving cell survival, and the attenuation of Aβ42‐induced NF‐κB activation. The gene discussed is NFKB1; the disease is Alzheimer disease.