This signaling pathway is impaired in COPD as although the expression of LC3 is increased in COPD patients and smokers with normal lung function compared to non-smokers controls, COPD patients also show an enhanced expression of p62 that is well-known to be a marker correlated to impaired autophagy and increased intracellular accumulation of damaged organelles and noxious molecules that usually are destroyed through the autophagic flux [17], suggesting that other autophagic mediators can have a key role in the modulation and in the effectiveness of intracellular autophagy. This evidence concerns the gene MAP1LC3A and chronic obstructive pulmonary disease.