In this regard, in mice with genetically-induced deletion of leptin receptors Db-/-), which are prone to consume excessive calories and develop obesity and insulin resistance, high levels of CML were trapped by the adipose tissue, while the deletion of RAGE reverted CML accumulation in adipose tissue, increasing its plasma levels, indicating a RAGE-dependent mechanism underlying endogenous AGE-induced obesity [97]. The gene discussed is LEPR; the disease is obesity due to melanocortin 4 receptor deficiency.