NLRP3 and COVID-19: A recent study reported that SARS‐CoV‐2 infection and replication in lung‐resident macrophages triggered the reactivation of NLRP3 inflammasome, leading to a hyperinflammatory state of the lungs and severe COVID‐19.[16] Treatments with caspase‐1 and NLRP3 inhibitors significantly attenuated inflammatory cytokines in vivo and in vitro, but promoted the production of SARS‐CoV‐2 particles, which poses a risk to the benefits from the systematic inhibition of the pathway.