Posttransfusion hepatitis of the non-A, non-B variety continues to be a significant problem in current hemotherapy. This disorder is many times more common than transfusion-associated disease caused by hepatitis B virus, cytomegalovirus, and Epstein-Barr virus, and also seems to be viral in origin. Several potential etiological agents have been implicated, but none has been identified with certainty, despite concerted efforts at doing so. Clinical disease is usually attended by few symptoms and signs, but evolution to chronic liver disease is distressingly common; over 50 percent of all cases of non-A, non-B posttransfusion hepatitis manifest this transition. Efforts at prevention of non-A, non-B hepatitis associated with blood transfusion have thus far been hampered by the lack of reliable laboratory markers for carriers of this disease, and controversy exists over the implementation of screening tests on blood donors, using such nonspecific indicators of possible viral carriage as serum alanine aminotransferase levels. It is probable, however, that simple measures such as more restrained blood usage, encouraged by greater educational efforts within the medical community, could be beneficial in minimizing the number of new cases of non-A, non-B posttransfusion hepatitis seen each year in the United States.