These findings illustrate the intricate interplay between leptin, GLP-1, and ERK1/2 signaling in the regulation of energy homeostasis and suggest potential targets for the treatment of obesity through the combined activation of GLP-1 and leptin receptors in the central nervous system, all of which can be modulated by alliin. The gene discussed is LEPR; the disease is obesity due to melanocortin 4 receptor deficiency.