19 reported that the FGF19 transgenic mice were resistant to adiposity and displayed increased metabolic rate. Furthermore, FGF21 has been implicated in the stimulation of glucose uptake as well as in the resistance to diet‐induced obesity 20. The subsequent in vitro studies demonstrated that the KLB acts as a co‐receptor for FGF19 and FGF21, both of which exhibited low affinity to their corresponding FGFRs 21, 22, 23. In addition, Adams and colleagues provided clear evidence regarding the involvement of KLB in regulating the metabolic processes of FGF19/21 in experimental animals 24, 25. The gene discussed is FGF21; the disease is obesity due to melanocortin 4 receptor deficiency.