This hypothesis is consistent with the findings of previous reports that both Gorlin syndrome patients with heterozygous loss-of-function PTCH1 mutations and Ptch1-deficient (Ptch1+/−) mice exhibited increased bone mass as adults and that osteoblast differentiation was accelerated in Ptch1+/− mouse cells [9]. This evidence concerns the gene PTCH1 and nevoid basal cell carcinoma syndrome.