Among other findings, they based their proposition on (i) that the elevated plasma levels of soluble uPAR in primary and recurrent FSGS were independent of the estimated glomerular filtration rates (eGFR) and (ii) that glomerular uPAR deposits activated podocyte αvβ3 and thereby drove foot process effacement leading to manifest proteinuric glomerular disease. This evidence concerns the gene PLAUR and focal segmental glomerulosclerosis.