Studies have shown that dysregulated wound healing is involved in the pathogenesis of desmoid tumor-like fibroblastic lesions.[28] In particular, the sporadic type of desmoid tumor is associated with CTNNB1 mutations, which dysregulate the β-catenin level and induce nuclear accumulation of β-catenin.[29,30] Recent molecular studies have demonstrated that mutational analysis for CTNNB1 is clinically significant for the diagnosis of desmoid tumors. Here, CTNNB1 is linked to desmoid tumor.