It has been shown previously that development of necrotizing enterocolitis (NEC), a leading cause of death from gastrointestinal disease in preterm infants, requires activation of TLR4 on enterocytes and that TLR4 activation by bacterial endotoxin LPS (lipopolysaccharide) inhibits enterocyte proliferation and leads to disease progression due to impaired β-catenin signaling after activation of the Akt-GSK3β signaling pathway [28]–[30]. This evidence concerns the gene AKT1 and necrotizing enterocolitis.