Although several studies show that knockout mice for the leptin gene or for STAT3, develop obesity, precisely because of altered activation of the previously described pathway, modulation of JAK-STAT finds itself at the center of a conflicting condition for another property that has emerged: the promotion of UCP-1 and the consequent induction of the browning phenomenon. The gene discussed is SOAT1; the disease is obesity due to melanocortin 4 receptor deficiency.