In line with these observations, our current findings indicated that genetic impairment of autophagic proteins Beclin-1 or LC3B, or chemical inhibition of autophagy either during CS-initiated sensitization or during elastin provocation significantly inhibited the bronchitis-like phenotypes in mice, reassuring the deleterious effect of autophagy in CS-induced epithelial injury. Here, MAP1LC3B is linked to bronchial disorder.