These factors: CD36 expression by other inflammatory cells and possible interaction of CD36 both with Tr-OxPLs and S. aureus add a complexity to the interpretation of animal experiments, which demonstrated the attenuation of Tr-OxPL/HKSA-induced endothelial dysfunction and ALI via the pharmacological and molecular inhibition of CD36. The gene discussed is CD36; the disease is endothelial dysfunction.