Tomlinson's group observed an increased energy expenditure level, a significant decreased fat mass, as well as resistance to diet-induced obesity in the transgenic mice.[3] Administration of recombinant FGF19 protein recapitulated most of these metabolic effects, preventing both high fat diet-fed and ob/ob mice from the impairment of glucose intolerance.[4] Although the molecular mechanisms still remain unclear, they believe that FGF19 may play a role in the pathogenesis of metabolic disorders. The gene discussed is FGF19; the disease is obesity due to melanocortin 4 receptor deficiency.