For example, reduction of caspase‐1 and IL‐1β through knockdown of NLRP3 in AD models can considerably eliminate Aβ‐42 (Wu et al., 2017), and functional loss of the NLRP3 inflammasome could diminish hyperphosphorylation and aggregation of tau by regulating tau kinase and phosphorylase (Dempsey et al., 2017). The gene discussed is IL1B; the disease is Alzheimer disease.