For example, changes in the splicing pattern of fibronectin can play a role in the pathogenesis of glomerulosclerosis and tubulointerstitial fibrosis by modulating the immune response and scar formation.[23] Further, Oltean et al. recently discovered that changes in splicing of anti-angiogenic VEGF-A isoforms are involved in the progression of diabetic nephropathy. Here, FN1 is linked to glomerulosclerosis.