Using human primary nasal epithelial cells from patients with CRS, including asthma patients and healthy controls, a recent study showed that RV-induced epithelial NLPR3 inflammasome activation could mediate IL-1β secretion, cell pyroptosis, and mucin production in airway epithelium through the DDX33/DDX58-NLRP3-caspase-1-GSDMD-IL-1β signaling axis, and these pathologic changes were relevant to virus-induced acute exacerbation [137]. This evidence concerns the gene NLRP3 and asthma.