This finding predicts that humans who are heterozygous for one of the obesity-predisposing mutant MC4R alleles will also be at risk and may develop symptoms – albeit at a milder level than homozygous carriers of two mutant alleles – because heterodimers of the mutant form will interfere with the physiological function of MC4R. The gene discussed is MC4R; the disease is obesity due to melanocortin 4 receptor deficiency.