PNLA potentially elicited ligand activity for PPAR-α and PPAR-δ as treatment with this FA upregulated the downstream target genes of PPAR-α and PPAR-δ involved in FA oxidation, including peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1α, mitochondrial uncoupling protein 3 (UCP3), carnitine palmitoyl-transferase 1B (CPT1b), acyl-CoA dehydrogenase medium chain (ACADM), and ACADL in the C2C12 myotubes cell line [34] and PBMCs from HCs and RA patients [5]. The gene discussed is ACADM; the disease is rheumatoid arthritis.