Preliminary information about the functions and physiological role related to feeding of MC3R and MC4R was provided by studies with the deletion of these MCRs in mice, which developed obesity, increased adipose mass, hyperphagia and lack of appetite control, in particular more pronounced in MC4R knockout (KO) mice rather than MC3R KO mice, even though mice lacking both receptors become significantly heavier than MC4R KO [11,16,65,66,67,68]. The gene discussed is MC3R; the disease is Obesity.