In vivo studies have suggested that the net influence of cortisol on lipolysis is highly dependent on prevailing insulin concentrations: cortisol has a more pronounced effect to induce lipolysis when insulin levels are low, e.g., during a pancreatic clamp or overnight, whereas rates of lipolysis may be reduced by cortisol when there is compensatory hyperinsulinemia, e.g., in Cushing's syndrome. The gene discussed is INS; the disease is hyperinsulinism.