This is functionally important in the context of DMD pathology because the transition of satellite cells from an HSP47−/ERTR7− to an HSP47+/ERTR7+ phenotype reflects a reduction in their myogenic capacity and an increase in their production of connective tissue proteins that may exacerbate the pathology of muscular dystrophy33 and lead to a reduction in the regenerative capacity of muscle over time40. The gene discussed is SERPINH1; the disease is Duchenne muscular dystrophy.