A previous study demonstrated that expression of CXXC5 is upregulated and is inversely correlated with that of β‐catenin in both haired and bald individuals.85 In mice, CXXC5 knockout or competitive peptide‐mediated disruption of the CXXC5‐Dvl interaction restores Wnt signaling and accelerates hair regrowth and wound‐induced hair follicle neogenesis.85 Similarly, targeting the CXXC5‐Dvl interaction with small molecules has been suggested as a new therapeutic approach for the treatment of anabolic osteoporosis.86, 87. The gene discussed is DVL1; the disease is osteoporosis.