The rationale for the proposed profibrotic growth factor-based methods relies on the observation that, in fibrotic muscles of human DMD patients and old mdx mice, TGFβ1 (and its downstream target CTGF) is present at high levels [22,44], correlating with the increased activation of Smad2/3 transcriptional mediators (see Figure S5 in Additional file 6). This evidence concerns the gene SMAD2 and Duchenne muscular dystrophy.