Also, mice lacking uPAR (plasminogen activator, urokinase receptor, PLAUR−/−) were protected from lipopolysaccharide- (LPS-) mediated proteinuria but developed disease after expression of a constitutively active αvβ3 integrin, suggesting the pathogenic role of uPAR signaling in the pathogenesis of proteinuric kidney diseases including FSGS [9, 45]. This evidence concerns the gene PLAUR and focal segmental glomerulosclerosis.