Mechanistically, sesquiterpene lactone bigelovin covalently binds to a cysteine residue of RACK1 and blocks NLRP3 oligomerization (active conformation), inhibiting the assembly of NLRP3 inflammasome, caspase‐1 activation, and IL‐1β production, which ultimately reduces ARDS severity. The gene discussed is NLRP3; the disease is acute respiratory distress syndrome.