The constructs made to identify co-chaperone binding in full-length SP-C mutants provided us with an opportunity to contribute strong support for the hypothesis that the BRICHOS domain acts in trans to chaperone the integration of SP-C’s unusual transmembrane region into the ER bilayer and revealed insights into folding defects for ILD-associated SP-C mutants and the autosomal dominant nature of this protein folding disease. This evidence concerns the gene SFTPC and interstitial lung disease.