In summary, the overexpression of Smad3 protein in NEC secondary to intestinal stenosis may promote intestinal fibrosis and participate in the development of secondary intestinal stenosis by promoting TGF-β1, NF-κB, and TNF-α protein expressions and inhibiting ZO-1 and VEGF protein expressions in the epithelial cells. This evidence concerns the gene NFKB1 and stricture.