IL1B and gastric ulcer: NSAIDs cause the activation of the cell causing the phosphorylation of factor IκB which is degraded followed by the release of NF-κB, which is introduced into the nucleus of the cell and causes the transcription of numerous proinflammatory mediators including iNOS, COX-2, TNF-α, IL-1β, IL-6, and IL-8 [50]; thus, the aggravation of the inflammatory process in the pathophysiology of gastric ulcers would be due to an overproduction of cytokines and inflammatory mediators.