These data are consistent with the previous ones appeared in literature and they could explain both the increased expression of LC3 in COPD as well as the ineffective autophagic flux characterizing COPD since the increased expression of these ATGs (such as ATG5, ATG7, and ATG4 protein family) involved in activation and recycling of LC3 can occur in an accelerated, uncoordinated and impaired autophagic flux. The gene discussed is MAP1LC3A; the disease is chronic obstructive pulmonary disease.