To test this possibility directly, using quantitative RT-PCR, we determined that the expression of TLR4 is significantly greater in the premature mouse and human compared with the full-term state and moreover, the expression of TLR4 is significantly elevated under conditions that are particularly relevant to the pathogenesis of NEC, namely, the presence of hypoxia and exogenous bacteria or LPS [72, 73]. Here, TLR4 is linked to necrotizing enterocolitis.