Although we tested several ATG proteins, a major part of these did not change between COPD patients and controls; however, these results may enhance these findings as the selective increase of mainly ATG4 family proteins can explain the unbalance on the autophagic flux with an excessive ATG4 activity and thus an ineffective intracellular autophagy, whereas a global increase of all ATG proteins including also LC3B should be correlated to an increased autophagic flux. The gene discussed is MAP1LC3B; the disease is chronic obstructive pulmonary disease.