Objective[|]Asthma is a chronic inflammatory lung disease. The renin–angiotensin system (RAS) targets several tissues and maintains fluid homeostasis. It is also known that RAS plays a role in inflammatory processes. Angiotensin-converting enzyme (ACE) and its product angiotensin II (AngII), which are the components of RAS, regulate the known effects of RAS. The other components of RAS, ACE2 and its product Ang 1–7, regulate the counter-effects of RAS. That is why the activation or inhibition of RAS can offer new therapeutic strategies for treating several diseases. We aimed to investigate the serum level of RAS components such as angiotensinogen (AGT), ACE, AngII, ACE2, and Ang 1–7 in asthma and control groups.[¤]Materials and Methods[|]This study was performed on 27 asthma and 23 healthy individuals. The serum levels of AGT, ACE, AngII, ACE2, and Ang 1–7 were measured by human enzyme-linked immunosorbent assay (ELISA) kits.[¤]Results[|]There were no statistically significant differences for the serum levels of AGT and ACE between the groups. The serum levels of AngII, ACE2, and Ang 1–7 were significanlty higher in the asthma group than those in the control group.[¤]Conclusion[|]Our results indicate that two tails of RAS, i.e., the ACE and ACE2 pathways, are activated in asthma compared to are activated more in the asthma group than in the control group. We suppose that the activation of ACE2 tail of RAS occurs because of the homeostatic balance requirements of this system. We believe that the activation of ACE2 pathway, in addition to the inhibition of the ACE pathway, can provide clinical benefits in treating asthma.[¤]