Therefore, in this study, we crossbred TRPV1 knockout mice with UCP1 knockout mice to generate TRPV1/UCP1 double knockout mice to determine the necessity of TRPV1-mediated Ca2+ influx to adipocytes in the maintenance of the BAT phenotype in this obesity model and investigate the possible mechanism accounting for obesity-induced hypertension. The gene discussed is UCP1; the disease is obesity due to melanocortin 4 receptor deficiency.