And the blood clot is used to basically coagulate the blood to form those clots on those cuts to basically prevent the leakage of blood out of that blood vessel. Now as I mentioned earlier, thrombin basically creates various different types of feedback loops and one of these positive feedback loops is shown on the board with the green arrow. So what happens is once throbin is activated it not only activates fibrinogen to form fibrin, it also goes back and stimulates factor A to basically continue to interact with factor nine to basically stimulate or to basically convert even more of these factor x inactive zymogen, factor ten into the active form. And so these two pathways along with all these different types of positive feedback loops basically greatly amplify the number of blood clots that we form. And so what happens is because of the quickness and the efficiency of this blood clot and cascade as a result of the correct functioning of all these different proteins and enzymes and pathways we're actually able to actually quickly seal off that cut, that rupture in the blood vessel. Now what happens in hemophilia is as I mentioned earlier, it's the intrinsic pathway that is actually impeded, that is actually affected.