In LPS-induced bone marrow macrophages and monosodium urate (MSU)-induced mouse arthritis models, andrographolide suppressed the activity of the NLRP3 inflammasome, and its mechanism in the treatment of gout mainly involved the downregulation of LPS-induced IKK, IκBα and NF-κB phosphorylation to inhibit IL-1β release, reduce NLRP3 and pro-IL-1β protein expression, induce HO-1 expression, reduce reactive oxygen species generation, reduce LPS/MSU-induced NLRP3 inflammasome assembly and cysteine Asparaginase-1 formation and attenuate MSU phagocytosis (Lo et al., 2021). The gene discussed is NLRP3; the disease is gout.