The following in vivo experiments further validated the protection of CPT1A overexpression in pulmonary fibrosis; however, the antifibrosis property of CPT1A was partly abolished by 3-MA, indicating that APN/CPT1A-mediated fatty acid metabolism exerted its protective role in IPF partly through activating autophagy. This evidence concerns the gene ANPEP and idiopathic pulmonary fibrosis.