While some of these changes in e2 carriers are consistent with better health profiles, increasing levels of APOC3 have been associated with increased risk for cardiovascular disease, and inhibition of APOC3 has been suggested as a possible therapeutic target.[28] Additional analyses are necessary, but considering the elevated level of APOC3 in e2 carriers, our results suggest that the elevated APOC3 level in patients with a metabolic disorder could be a compensatory mechanism rather than a causative mechanism of the disease. This evidence concerns the gene APOC3 and metabolic disease.