In metabolic diseases, such as obesity, a shift in the adipocyte phenotype from a protective profile to an imbalanced production of proinflammatory, pro-oxidant and profibrotic adipokines, such as leptin, resistin and visfatin, has a direct local effect in the pathogenesis of arteriosclerosis via an increased rigidity of the wall, contributing to the hypertension found in the obese patient [42]. The gene discussed is LEP; the disease is obesity disorder.