ACE2 and pulmonary fibrosis: A possible explanation could be the severe down regulation or absent expression of ACE2 during the proliferation of active type I pneumocytes during lung fibrosis, that appear to replace the damaged alveolar type II pneumocytes (111), in addition to a decrease in ACE2 representation in cell surface by internalization after its binding to SARS-CoV-2, and/or the possible decrease in enzymatic action by glycation.