This is also similar to the results of human studies examining idiopathic pulmonary fibrosis (IPF; [74,82]) where genetic-based overproduction of Muc5b and surfactant proteins (e.g., SftpA1and SftpC) contributes a strong muco-ciliary component in the cycle of dysfunctional response/repair leading to pathology that bears a remarkable similarity to the α7E260A:G mouse. This evidence concerns the gene SFTPC and pulmonary fibrosis.