However, a study by Hutchins et al. utilizing a CLP model of sepsis, showed that sepsis caused an increase in expression of PD-L1 on liver sinusoidal endothelial cells, increased liver tissue vascular permeability and edema, and genetic deficiency of PD-L1 restored vascular barrier integrity and attenuated endothelial cell apoptosis [52]. The gene discussed is CD274; the disease is Sepsis.