In seeking to define whether negative regulatory strategies for TLR4 within the newborn intestinal epithelium could participate in the pathogenesis of NEC, we focused on the intracellular chaperone heat shock protein 70 (Hsp70), to determine whether perhaps Hsp70 could negatively regulate TLR4 signaling within enterocytes and by extension, whether a loss of Hsp70 could lead to NEC development through uninhibited TLR4 activation. This evidence concerns the gene TLR4 and necrotizing enterocolitis.