With this goal in mind, investigators strive to generate overt gut necrosis, severe histological damage, and marked elevation of inflammatory mediators, such as inducible nitric oxide synthase (iNOS) and Toll-like Receptor 4 (TLR4), which have consistently been shown to be drastically elevated in animals with NEC and in intestinal sections resected from babies requiring bowel resection for necrosis [14], [15]. The gene discussed is TLR4; the disease is necrotizing enterocolitis.