Other studies have shown that NLRP3/IL-1β is critically involved in rodent neonatal hyperoxia-induced lung injury [18] and caspase-1 inhibition was shown to inhibit inflammasome assembly and atherosclerosis by alleviating mitochondrial damage and boosting mitophagy using cell cultures and an adolescent murine model exposed to high-fat diet to facilitate the formation of atherosclerotic lesions [43]. The gene discussed is IL1B; the disease is atherosclerosis.