This case presentation demonstrates the clinical picture of a patient with Kambô-related severe hyponatremia, diffuse cerebral edema, and subsequent brain death, highlighting the dangerous pathophysiological cascade triggered by Kambô envenomation: phyllocaerulein and phyllomedusin stimulate CCK-A and NK1 receptors, respectively, inducing parasympathetic-driven emesis, diarrhea, and salivary hypersecretion, while sauvagine activates CRF1 receptors, promoting sympathetic-adrenal activation and inappropriate ADH release. The gene discussed is AVP; the disease is brain edema.