We have observed the accumulation of both substrates for enoyl-CoA isomerase activity (e.g. DCI) as well as dicarboxylic acids well known to reflect alternative fatty acid catabolism through ω-oxidation pathways, findings consistent with our predictions regarding an important role for DCI, the essential link between saturated and unsaturated β-oxidation, in the impaired mitochondrial fatty acid catabolism occurring during HCV-associated liver disease progression [28]. This evidence concerns the gene ECI1 and liver disorder.