CFTR and cystic fibrosis: Possible pathophysiologic mechanisms for MI include a lack of CFTR function in the intestinal epithelial cells causing (a) abnormal pH or HCO3− concentration in the intestinal lumen, (b) decreased hydration of the meconium making it more solid than in the non-CF intestine, (c) abnormal mucin cross-linking, (d) CFTR-dependent smooth muscle dysfunction causing intestinal dysmotility, or (e) CFTR-dependent intestinal growth anomalies leading to atresia, malrotation, or other structural abnormalities.