SMAD2 and fibrosis: Using mice subjected to cardiac pressure overload stimulation via transverse aortic constriction surgery, Khalil et al. showed that TGF-β-treated Smad3- and SMAD2/3-deleted fibroblasts had a significant reduction in fibroblast marker genes (POSTN, COLLAL and COL3AL) in primary cardiac fibroblasts, indicating that deletion of SMAD3 from newly activated fibroblasts may significantly attenuate cardiac fibrosis response [80].