CPT1a inhibitor ETO as well as oleic acid, a fatty acid that is upregulated in the plasm of IPF patients [36] and has pro-fibrotic effect [37], can inhibit the anti-fibrotic effect of mitoQ, demonstrating that mtROS activated LF by dysregulating PPARα/CPT1a-related FAO. The gene discussed is PPARA; the disease is idiopathic pulmonary fibrosis.