IPF lung fibroblasts also have constitutively more LXRα protein (and upregulated LXRα and ABCA1: IPF data repositories GSE205233 and GEOD-2420634), and greater LXR-dependent profibrotic activation that was normalized by miR-155 overexpression, LXRa gene silencing, or metabolic antagonism of LXRα activity using 22(S)HC. This evidence concerns the gene ABCA1 and idiopathic pulmonary fibrosis.