It is understandable that a period of approximately 40 years separated the discovery of vitamin K and the demonstration of its biochemical role. As the metabolic pathway leading to the synthesis of proteins was unknown when the vitamin was discovered, it was difficult to elucidate the mechanism by which a low-molecular-weight lipophilic compound such as vitamin K could influence either the activity or the amount of a specific plasma protein such as prothrombin. Various roles for the involvement of vitamin K in prothrombin production were, however, postulated. In the 1930s, Dam, Schonheyder, and Tage-Hansen postulated [1] that vitamin K, or a portion of it, might be part of the prothrombin molecule, and in the 1950s Martius and Nitz-Litzow proposed [2] that vitamin K might be involved in mammalian electron transport and that a vitamin K deficiency could lead to a low cellular ATP level and an inability to maintain normal physiological concentrations of proteins with a rapid turnover rate. In the mid 1960s, as an understanding of protein synthesis and its control was being developed, Olson [3] postulated that the rate of prothrombin synthesis is regulated by an effect of vitamin K on DNA transcription. In the late 1960s, Johnson [4] proposed that vitamin K was a precursor of a protein cofactor that was involved in the removal of prothrombin from polysomes and guiding it to its biologically active tertiary structure. Little evidence to support these early hypotheses was ever developed.