Ali et al. (30) further demonstrated increased IFABP at the time of clinical NEC in neonates after CHD surgery, and Owens et al. (31) reported higher postoperative IFABP together with tight-junction proteins (claudin-2, claudin-3) in children who developed feeding intolerance, strengthening the biological plausibility of IFABP as an epithelial-injury marker. This evidence concerns the gene CLDN3 and coronary artery disorder.