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. The gene discussed is CLDN2; the disease is coronary artery disorder.