TMPRSS2 and pulmonary fibrosis: Respiratory and alveolar epithelial cells, particularly type II alveolar epithelial cells, are infected by SARS‐CoV‐2 and hijacked to execute rapid viral expansion because of their high expression of ACE2 and transmembrane protease serine 2 (TMPRSS2).[115, 116, 117, 118, 119, 120] SARS‐CoV‐2 accumulation induces a persistent viral inflammatory response and apoptosis of recruited lymphocytes, thus accentuating the cytokine storm and ultimately triggering ARDS and lung fibrosis injury.[121, 122, 123, 124]