Positive factors dominated by the angiotensin-converting enzyme (ACE)/angiotensin II (AngII)/AngII type 1 receptor (AT1R) axis have been reported to be activated during pulmonary fibrosis and EMT, while negative regulators dominated by the ACE2/angiotensin 1–7 (Ang1–7)/Mas axis are reduced during fibrosis and EMT [22]. This evidence concerns the gene ACE2 and pulmonary fibrosis.