Even though increased levels of clusterin, alpha-1 antitrypsin and orosomucoid 1 in CF piglets could indicate that their development is altered compared to WT piglets, the fact that apolipoprotein A1 was also increased indicates that because acute phase proteins produced in the liver were increased in newborn CF piglets, they have mounted a systemic inflammatory response, further strengthening the hypothesis that inflammation is a result of stagnant mucus and lack of CFTR function, not bacterial infection [52]. This evidence concerns the gene CFTR and bacterial infectious disease.