Our data suggest that this unusual dissociation of TGF-β activation/inflammation and myofibroblast activation/fibrosis/sclerosis may relate to chronic and long-term anti-angiogenic side effects of the TSP-2 therapy on the renal microvasculature during disease course, which has not been seen during short-term TSP-2 gene therapy in anti-Thy1 nephritis [15]. The gene discussed is TGFB1; the disease is nephritis.