To confirm our finding that cav-1 level is transcriptionally low due to FoxO3a suppression in IPF fibroblasts on polymerized collagen, we utilized a reporter construct that contains consensus FoxO3a binding sites within the promoter of luciferase gene (FHRE-Luc) [46], and luciferase activity was measured in IPF and control fibroblasts expressing wild type FoxO3a, dominant negative FoxO3a or GFP. Here, CAV1 is linked to idiopathic pulmonary fibrosis.