The pathomechanism of hyponatremia in GBS has not been clearly elucidated, although multiple theories have been discussed including impaired autonomic nervous function involving the afferent fibers from vascular stretch receptors [5], resetting of the osmostat [15], increased sensitivity of distal tubular and collecting duct ADH receptors, and ADH-independent mechanisms [16]. The gene discussed is AVP; the disease is Hyponatremia.