The loss of Magel2 disrupted the normal balance of expression, internalisation and degradation on the surface of LepR cells and resulted in leptin resistance and obesity.[10] It was found that the related pathway of leptin in Magel2 was not only involved in the mechanism of obesity but also in the abnormal expression of autistic behavior. This evidence concerns the gene LEPR and obesity due to melanocortin 4 receptor deficiency.