A possible explanation could be the greater affinity of the somatostatin receptors expressed both on pituitary lesion and at intestinal level in well controlled patients with a consequent greater risk of cholelithiasis evolution, principally because of reduction of cholecystokinin release from the small intestine [3] and inhibition of the usual prandial relaxation of the sphincter of Oddi, motility, and emptying of the gallbladder [4]. The gene discussed is CCK; the disease is cholelithiasis.