Our findings suggest that increased vascular TGF-β1 induces PAD myofibrosis by activating fibroblasts that proliferate and either stay locally around the microvessels or migrate between myofibers and around myofascicles into areas of myofiber degeneration, thus being responsible for the perivascular and endomysial/perimysial fibrosis we and others [48, 49] have shown in the affected leg muscles of PAD patients. This evidence concerns the gene TGFB1 and peripheral arterial disease.