Uncertainty surrounds how dysbiosis in gut microbiota affects NEC pathogenesis, however, results of piglet, mice, and human studies suggest that stimulation of immature enterocytes by Gram-negative lipopolysaccharide through Toll-like receptor 4 (TLR4) can lead to over-activation of inflammatory responses in the intestines of premature infants and lead to bowel damage and NEC progression [19,20]. This evidence concerns the gene TLR4 and necrotizing enterocolitis.