Interestingly, in patients aged 4–44 months suffering congenital nephrotic syndrome of the Finnish type manifested by proteinuria, fibrosis, and inflammation, despite the severe tubulointerstitial fibrosis, tubular epithelial cells did not show transition into myofibroblasts based on vimentin, SMA, collagen, or matrix metalloproteinases 2 and 9 (MMP-2 and -9) expression (Kuusniemi et al., 2005). The gene discussed is MMP2; the disease is familial nephrotic syndrome.