In SAT, increased mass in Cfb−/− rats was associated with increased Fasn and reduced Pgc1a expression, consistent with the function of Fasn as an insulin-sensitive fatty acid synthase, the role of Pgc1a in stimulating fatty acid oxidation, and the known upregulation of FASN in human obesity and type 2 diabetes mellitus.24 These changes seemed to override the increases in Aco1 and Ucp1 expression observed in Cfb−/− rats, which would be expected to reduce adipocyte mass through increased trichloroacetic acid cycle activity and thermogenesis. The gene discussed is CFB; the disease is Obesity.