This spontaneous literature case was received from a physician on 09-Aug-2017. This case concerns a 42-year-old adult female patient. On an unspecified date, at the age of 36 years the patient had unilateral optic neuritis from which she had recovered. On an unspecified date, at the age of 42 years optic neuritis recurred. Brain MRI (Magnetic Resonance Imaging) showed multiple T2-hyperintense white matter lesions, a gadolinium-diethylenetriamine penta-acetic acid-enhancing lesion and multiple sclerosis (MS) was diagnosed. The patient was treated with methylprednisolone 1 g/daily intravenous (IV) for 5 days. Concomitant medications included norethindrone/ethinyl estradiol with iron, vitamin D, calcium and vitamin B12. The patient did not take supplements or abuse alcohol. Approximately 3 weeks later, the patient was started on Non-company suspect Glatopa [generic glatiramer acetate (GA), daily injection, dose, route, anatomical location, batch number and expiry: not reported] for relapsing-remitting MS. At the time she began GA, the patient received INN Flu Vaccine Seasonal (dose, route, anatomical location, batch number, expiry date, trade name and manufacturer: not reported) and Non-company suspect meningococcal oligosaccharide vaccine (dose, route, anatomical location, batch number and expiry: not reported). Because of symptoms of injection pain, fatigue, nausea and constipation, the patient discontinued GA after 13 daily injections. The following day, the patient developed worsening nausea with vomiting, dyspnea with exertion, anorexia, fatigue, dark urine and jaundice. The patient was found to have elevated liver function tests was 1,188 U/L, alanine transaminase was 1,879 U/L, alkaline phosphatase was 177 U/L and total bilirubin was 3.6 mg/dL, which were compared with normal values recorded on 17-Feb-2016 (just 1-month prior to GA). The following laboratory values were negative or normal: HAV IgM, HBsAg, HBcAg IgG, HCV RNA, HCV antibody, HEV IgM, EBV IgM, CMV IgM, HIV, HSV PCR, urine toxicology screen, acetaminophen levels, ANA and anti-smooth muscle antibody, HAV IgG, HBsAb, HEV IgG, and EBV IgG were positive. Twenty-four-hour urine copper: 193 mg/24 h was presumed to be elevated secondary to acute liver injury. A liver biopsy showed severe portal, interface and panacinar, lymphocyte-predominant inflammation, with confluent necrosis, numerous apoptotic hepatocytes, and central perivenulitis. This histologic picture along with the clinical presentation and temporal profile was consistent with drug-induced liver injury. The bile ducts were intact and there was no significant ductular reaction. Steatosis, cholestasis and fibrosis were not present. The patient was treated with IV corticosteroids followed by a several months taper of prednisone for possible autoimmune hepatitis. The patient's liver function tests normalized within 2 months and these were recorded till 13-Jun-2016 (102 days following the start of GA treatment). The reporter stated that, due to generic GA use the patient had hepatocellular injury pattern without hyperglobulinemia but autoimmune hepatitis could occur. Based on patient's negative autoimmune markers, lack of plasma cells on biopsy and resolution of liver injury on a rapid prednisone taper. It was unlikely that the patient had autoimmune hepatitis. The administration of influenza and meningococcal vaccines seemed unlikely to be contributory because neither vaccine was hepatotoxic. Seven years prior to the diagnosis of MS, the patient had a history of transaminitis, which was attributed to a viral etiology (associated with serologic evidence of prior hepatitis A and hepatitis E virus exposure), followed by many years of normal liver enzymes. It was reported that, the generic GA was only recently available for clinical use in MS and was the likely cause of acute liver injury in the present case report and heightened awareness of possible liver dysfunction.