On the other hand, the conversion of Ang II into Ang 1-7 by ACE2 counteracts the action of Ang II in pulmonary fibrosis, so that a depletion of ACE increases collagen deposits in the extracellular matrix, resulting in an imbalance between ACE/ACE2 that has been related to the severe progression of respiratory diseases (68), as seen in patients with chronic obstructive pulmonary disease, where there is greater ACE activity (60). This evidence concerns the gene ACE and chronic obstructive pulmonary disease.