The fact that treatment of hyperthyroid patients with propranolol, a β adrenoceptor antagonist, corrects the thyrotoxicosis-induced hypercalcemia (42) and decreases the urinary excretion of hydroxyproline, a biochemical marker of bone resorption (43), support a possible TH-SNS interaction to control bone remodeling, in addition to suggest that this interaction depends on the β-AR signaling pathway. This evidence concerns the gene TH and thyrotoxicosis.