Besides, in circulating monocytes from patients with severe asthma, impaired autophagy is concomitant with highly activated NLRP3 and mitochondrial ROS accumulation; otherwise, restoration of impaired autophagy restrains NLRP3-driven release of IL-1β and IL-18 and attenuates airway inflammation and severe asthma phenotypes [54]. Here, NLRP3 is linked to asthma.