Non-insulin dependent diabetes mellitus (NIDDM) increased the propensity to gastric ulceration by enhancing offensive, acid-pepsin secretion and gastric mucosal free radicals, lipid peroxidation (LPO), nitric oxide (NO) and decreasing mucosal glycoprotein and antioxidants, superoxide dismutase (SOD) levels [10]. The gene discussed is SOD1; the disease is type 2 diabetes mellitus.