Given that COX-1 inhibitors (aspirin, indomethacin, and other NSAIDs) are known to induce gastritis [46] and potent NOS inhibitors (e.g., NG-Nitro-L-arginine methyl ester) exacerbate the EtOH-induced gastric ulcer index by up to 2-fold [47], we considered the possibility that COX-2 activity or COX-2-mediated levels of PGE2 could play a pathophysiological role in the generation of EtOH/HCl-induced stomach inflammation. This evidence concerns the gene NOS2 and gastritis.