Upregulation of Wnt16 induced by estrogen and progesterone treatment in uterine leiomyoma stem cells could promote the growth of uterine leiomyomas through activating the canonical Wnt pathway in a paracrine manner (138), and the enhanced β-catenin activities initiated by Wnt16 in prostate cancer cells could promote the malignant phenotypes and chemoresistance through preventing cell death (139). This evidence concerns the gene WNT16 and Familial prostate cancer.