SMAD7 and glomerulosclerosis: Using TGF-β transgenic mice and cultured murine podocytes treated with TGF-β, the authors demonstrated that both TGF-β and SMAD7 cause apoptosis of the podocytes but with a different mechanism: while TGF-β activates of mitogen-activated protein (MAP) kinase p38 and classic effector caspase-3, SMAD7 inhibits the NF-κB pathway (nuclear factor kappa-light-chain-enhancer of activated B cells), enhancing the apoptotic activity of TGF-β and therefore the development and progression of glomerulosclerosis [78].