Although the pathogenesis of NEC remains unclear, genetic, nutritional, and environmental risk factors that favor deviant interactions between the intestinal mucosa and gut microbiota portend NEC vulnerability.1, 2, 3, 4 Animal models suggest that aberrant activation of intestinal Toll-like receptor 4 (TLR4), a sensor of lipopolysaccharide derived from gram-negative bacteria is a central event in NEC pathogenesis, and TLR4-/- mice are protected against experimental NEC.5 Here, TLR4 is linked to necrotizing enterocolitis.