We draw the conclusion that CO released from its pharmacological donor, CORM2, protects against indomethacin-induced gastric ulcer through a variety of mechanisms, including activation of the NRF2/HO-1 pathway, a decrease in oxidative stress, lipid peroxidation through a reduction of NO and MDA, an increased COX-1, and a decrease in proinflammatory COX-2. Here, NFE2L2 is linked to gastric ulcer.