VWF and Sepsis: Specifically, ROK also (i) maintains active binding of the integrin GPIIbIIIa to fibrin and vWF [54,55], and it has been identified that activation of GPIIbIIIa is decreased in patients with sepsis [13]; (ii) mediates vesicle trafficking within platelets independent of MLCP [56-59]; (iii) is essential for TxA2- and thrombin-induced granule secretion [32,60] and (iv) modulates actin assembly and polymerisation in the dynamic regulation of microtubule coils [61-63] and formation of stress fibres [64].