VWF and Sepsis: In interaction with adhesion protein such as von Willebrand factor (vWF), activation of platelet integrin affinity was enhanced via MAPK/ERK pathway in a cGKI mechanism, while MAPK-mediated activation of platelet integrin αIIbβ3 require signaling via platelet GPIb-IX receptor.254 In addition, insufficient degradation of vWF due to ADAMTS13 deficiency might have enhanced thrombosis in sepsis and mimic certain clinical presentation of thrombotic thrombocytopenia purpura, supported by evidence of low levels of ADAMTS13 and association with DIC severity.255,256