At present, regarding the findings of Andre et al., as well as proving the affirmative inscription of the ACE2-Ang1-7-Mas receptor axis in controlling and suppressing inflammation and pulmonary fibrosis (27), we hypothesized that the increment of serum ACE2 concentration is induced by enhancement of pulmonary expression of this protein and also the body's compensatory mechanisms to prohibiting of the destructive effects of angiotensin 2 and related organs such as lungs and heart (48,49). The gene discussed is ACE2; the disease is pulmonary fibrosis.