These results indicate that the increased β-catenin binding on the Fbxo32 and Trim63 promoters does not antagonize canonical Wnt signaling and there is no apparent competition of β-catenin between the promoters of atrophy-related genes and the canonical Wnt targets, suggesting that Dkk3-induced muscle atrophy is not dependent on canonical Wnt signaling. The gene discussed is TRIM63; the disease is muscle atrophy.