Introduction: Drug-induced liver injury (DILI) is a major cause of iatrogenic illness, and may present with an array of histologic signatures. Establishing a diagnosis of DILI requires a careful exclusion of other etiologies and an awareness of the hepatotoxicity profile of suspected agents. Case: A 70-year-old man with a history of HTN, CAD, AF, and BPH was referred for a six-day history of intense pruritus, associated with jaundice, dark urine, and acholic stool. He denied any abdominal pain, weight loss, recent travel, fevers/chills, or sick contacts. Physical exam revealed a jaundiced patient with no cutaneous stigmata of chronic liver disease, and no hepatosplenomegaly, ascites, or asterixis. On presentation, his LFT's were as follows: T bili 7.5, D bili 4.6, AST 34, ALT 45, ALP 232, GGTP 63, alb 3.8, and normal INR. Serologies revealed a negative HAV IgM, HBSAg, HB core IgM, HCV PCR, ANA, SMA, AMA, anti-LKM, P-ANCA, ACE, and normal immunoglobulins. Doppler U/S revealed a normal liver morphology with a small hepatic cyst, patent hepatic vessels, normal gallbladder, no biliary ductal dilation and no hepatosplenomegaly or ascites. MRCP revealed a normal biliary tree with no pruning. Within 10 days of presentation, his T bili peaked at 20.9 with an ALP of 274. On further inquiry, the patient recalled a two-week course of amoxicillin/clavulanate (AugmentinTM) for a URI, with his symptoms beginning one week after discontinuation of the antibiotics. A liver biopsy revealed mild cholestasis, spotty necrosis/apoptosis, lymphocyte, neutrophil, and eosinophil infiltration consistent with a drug-induced hepatitis. There was no bile duct damage, ductopenia, granulomas, or fibrosis. The patient was prescribed cholestyramine four g BID for pruritus, and urso 250 mg BID. Within eight weeks, his LFT's had completely normalized. Discussion: Amoxicillin/clavulanate- induced DILI is estimated to occur with an incidence of 17/100,000 prescriptions, and the clavulanic acid component is the likely injurious agent. This idiosyncratic reaction is thought to be immunoallergic in origin, and autoantibody formation is uncommon. Men over 50 years of age and prolonged/repeated courses of AugmentinTM are associated with an increased risk of DILI. Although cases of acute liver failure and chronic ductopenia have been described with AugmentinTM, a delayed cholestatic or a mixed cholestatic-hepatocellular liver injury pattern is the norm, and usually resolves within two months. Despite our patient being an elderly male who developed marked jaundice, his course was ultimately benign, with full resolution of symptoms.