In conclusion, a schematic representation of the proposed anti-inflammatory effects mediated by GSNOR inhibition in asthma is depicted in Fig. 7, where the inhibition of GSNOR (which is over-expressed in inflammatory states and asthma) using GSNOR inhibitors will increase steady-state levels of S-nitrosoglutathione and thus inhibit inflammation and AHR. The gene discussed is AHR; the disease is asthma.