These results, plus those of earlier studies [32], highlight the potential of SOD3 to be a major player in the regulation of laminin α4 and laminin α5 in the endothelial BM of tumor vasculature, shifting the laminin α4/α5 balance towards a phenotype observed in postcapillaries at sites of leukocyte extravasation. The gene discussed is SOD3; the disease is neoplasm.