SFTPC and pulmonary fibrosis: With no alterations in autophagy and pulmonary fibrosis — likely due to low expression levels of SP-C(I73T) — findings in the SftpcI73T knock-in mouse model are consistent with previous studies demonstrating abnormal trafficking and processing of the mutant protein, and the knock-in mouse model is suitable for study of the primary effects of SP-C(I73T) expression in vivo.