Our data, together with others [5, 11, 30], who have used the same cell-based assays here employed provide epidemiologic evidence produced in free-living populations which validates previous basic science and clinical research on the role of mitochondrial dysfunction in the pathophysiology of diabetes [5, 7, 25, 26, 29, 30], especially in the presence of greater AhR activation, thus strengthening the contention that POPs cause diabetes and providing a causal pathway for their action. The gene discussed is AHR; the disease is diabetes mellitus.