Mouse models and IPF lung fibroblasts had constitutively increased LXRα transcription when deregulated from homeostatic miR-155, associated with LXR-dependent excessive fibrotic phenotype mediated by increased TGF-β, arginase, and collagen production that could be mitigated by LXR antagonist (Fig 6). This evidence concerns the gene TGFB1 and idiopathic pulmonary fibrosis.