Interestingly, in disease conditions that are likely associated with thrombin-induced endothelial permeability impairment, such as sepsis or trauma, systemic CXCL12 concentrations have been reported to increase to levels within the range of the EC50 for CXCL12 to attenuate thrombin-induced barrier function impairment in our permeability assays [58–60]. The gene discussed is CXCL12; the disease is Sepsis.