It has been shown that the knockdown of Rack1 in microglia in vitro decreased the production of LPS‐induced pro‐inflammatory cytokines.[33] Moreover, Rack1 was identified as a component of NLRP3 complexes in macrophages, playing an essential role in NLRP3 inflammasome activation.[23] Furthermore, NLRP3 deficiency in APP/PS1 mouse models was shown to reduce Aβ deposition, skew microglial cells toward an M2 phenotype, and alleviate cognitive impairment,[34] suggesting that Rack1 might also be involved in microglial activation and AD pathology. The gene discussed is NLRP3; the disease is Alzheimer disease.