Because GrB cleaves and destroys VWF pro-hemostatic activity in vitro[12], [16], this study], it will be of future interest to study whether GrB also inactivates VWF in vivo and thereby can be used as replacement for ADAMTS13 in diseases like TTP and/or during infection (where also lower ADAMTS13 levels are observed). The gene discussed is ADAMTS13; the disease is infection.