Evidence is provided for the existence of at least two types of hereditary factor VII deficiency. In one type there is synthesis of a protein which neutralizes a factor VII antibody but lacks coagulant activity. In the second type, no factor VII antibody neutralizing material is present. Evidence is also provided for the existence of two types of acquired factor VII deficiency. Apparently, low factor VII activity in liver disease results from decreased synthesis of factor VII protein. In contrast, warfarin administration or vitamin K deficiency leads to the synthesis of factor VII protein that lacks clotting activity.