The accumulation of acetyl-CoA further influences the lipid metabolism of CAFs by reprogramming the CXCL5–CXCR2 axis.[52] It is therefore speculated that the increased risk of IPF associated with Isovalerylcarnitine (C5) may be attributed to the disruption of lipid metabolism in CAFs through the regulation of key genes in the lipid metabolism pathway. The gene discussed is CXCR2; the disease is idiopathic pulmonary fibrosis.