TGFB1 and renal fibrosis: Despite this antagonism, SMAD2, in the same way as SMAD1/5/8 and SMAD7, was found to play a protective role against hepatic and renal fibrosis [75,76], even though TGFβ and BMPs can also synergistically activate different intracellular non-SMAD mediators (such as HIPK2 and TAK1) to activate p38 and JNK and thereby cause apoptosis, or alternatively Limk1 and Limk2 to inhibit cofilin, an event that results in F-actin polymerization, that in turn contributes to EMT [77].