Further, using the model of experimental glomerulonephritis in rats, Huang and colleagues showed that administration of a mutant human PAI-1 (PAI-1R) that binds to Vn normally but does not inhibit plasminogen activators, conferred protection against glomerulonephritis, while a PAI-1 mutant (PAI-1K) that has defective Vn binding but inhibits proteases normally, does not bring any benefit [44,45]. This evidence concerns the gene VTN and glomerulonephritis.