Further, the above factual components demonstrate that it is impossible to correctly redefine both “microthrombosis” and “macrothrombosis” using the contemporary hemostatic theory which is based on sequential activation via the extrinsic coagulation cascade initiated by the TF–FVIIa complex alone, [11], as well as fibrin clot disease of acute promyelocytic leukemia (APL) [39]. The gene discussed is TF; the disease is acute promyelocytic leukemia.