Deficient autophagy was associated with increased NLRP3 inflammasome assembly and culminated caspase-1 activation as observed in sepsis, enabling enhanced cleavage of pro-IL-1β and pro-IL-18 into their biologically active forms IL-1β and IL-18 in DSS-treated UVRAGFS mice colons (Fig. 4f–h). The gene discussed is NLRP3; the disease is Sepsis.