Deficiency of TIMP3 led to extensive cardiac fibrosis through activation of TNF-α, TGFβ1 and downstream molecules Smad2/3 after pressure overload in mice, which could be inhibited by a TGFβ1 neutralizing antibody (Table 1) (Kassiri et al., 2005; Kassiri et al., 2009). This evidence concerns the gene TGFB1 and fibrosis.