VWF and Sepsis: At the same time, endothelial activation, observed during sepsis, leads to the appearance of or increase in surface molecules, such as von Willebrand factor (vWF), E-selectin and integrins αVβ3, encouraging interaction with platelets and leading to their activation, while decreasing anti-adhesive inhibition pathways, thus favoring the risk of thrombosis (Romo et al., 1999; Kaplan and Jackson, 2011; Figure 1).