A consistent effect was observed in vivo, as hearts subjected to MI and treated with the anti-BMP1.3 antibody showed reduced levels of Tgfβ expression, reduced phospho-Smad2 accumulation in fibroblast nuclei within the scar, and reduced expression of the TGFβ target genes Col1a, Lox, Ctgf and Fn (Fig. 2f, g). Here, SMAD2 is linked to myocardial infarction.