Inhibition of the enzyme S-nitrosoglutathione reductase (GSNOR; EC 1.2.1.46) affects the metabolism of S-nitrosoglutathione and the maintenance of nitric oxide (NO) homeostasis. GSNOR is a zinc-dependent, NAD+- and NADH-dependent, medium chain alcohol dehydrogenase (ADH), but shows only modest affinity towards alcohols. Rather, the enzyme is also known as formaldehyde dehydrogenase, and as such, it targets GSNO in order to reduce its nitroso group into an unstable S-hydroxylaminoglutathione intermediate. Inhibition of GSNOR by N6022 (Axon 1822) and related compounds has shown safety and efficacy in animal models of asthma, chronic obstructive pulmonary disease, and inflammatory bowel disease[1].