As an independent confirmation, we also treated wild type mice with the Hh antagonist Gant61 (Supplementary Fig. 2a) and found a decrease in myofiber CSA 7 days post CTX injury (Supplementary Fig. 2b) similar to loss of Dhh. Thus, endogenous Hh activation, via DHH, is critical for myofiber regeneration after an acute injury. The gene discussed is DHH; the disease is cerebrotendinous xanthomatosis.