CCKA receptor-deficient mice and rats 31,65, PrRP-deficient mice 18 and oxytocin receptor-deficient mice 66 (Fig. 7) all show an increased meal size and late-onset obesity, suggesting the importance of the CCK–PrRP–oxytocin pathway in the control of food intake, especially in the termination of each meal. The gene discussed is CCKAR; the disease is Obesity.