A 6 year old, castrated male, Dalmatian presented to the Cornell University Hospital for Animals’ Emergency Service for further evaluation of chronically elevated liver enzymes and jaundice. On presentation, the patient was icteric and was hypersalivating. His problem list included: hyperbilirubinemia, elevated ALT/AST, polyuria, polydipsia, ptyalism, inappetence, lethargy, weight loss and historical urate uroliths. Prioritized differential diagnoses included hepatitis due to autoimmune, copper-associated, or infectious causes, with copper-associated hepatopathy most likely given the signalment. Abdominal ultrasound revealed diffuse nodular hepatopathy and probable gallbladder dysmotility. Unfortunately, despite supportive care and plasma transfusion, the patient quickly deteriorated, developing disseminated intravascular coagulation and neurologic abnormalities. Euthanasia was elected and necropsy revealed severe copper-associated hepatopathy with micronodular cirrhosis. Copper accumulation was noted to be the primary driver of parenchymal extinction, hepatocyte loss, and regeneration. This paper will discuss the pathophysiology of copper-associated hepatopathy as well as breed predilection, methods of diagnosis and treatment options.