The poor evolution of AHA has been associated with the presence of high titers of inhibitor autoantibody, the low initial activity of coagulation FVIII, immunoglobulin A (IgA) autoantibody against FVIII, the coexistence of malignancy, and low World Health Organization performance status scale [5,6,10,11]. This evidence concerns the gene F8 and autoimmune hemolytic anemia.