Further, they have demonstrated that this improvement in steatosis involves an increased expression of transcriptional factor PPAR-α and two rate limiting enzymes, namely, acyl-CoA oxidase-1 (ACOX1) and carnitine palmitoyltranferase-1 (CPT1), which are critical to mitochondrial β-oxidation [64]. The gene discussed is ACOX1; the disease is steatosis.