Although nicotine contributes to the development of cardiovascular and pulmonary disease in the long term, it has an effective influence on the homeostasis of RAS by upregulating the angiotensin-converting enzyme (ACE)/angiotensin (ANG)-II/ANG II type 1 receptor axis and downregulating the compensatory ACE2/ANG-(1-7)/Mas receptor axis [20]. This evidence concerns the gene ACE and lung disorder.