Mechanistically, those antitumor effects caused by TNKS inhibition or knockdown were associated with increased AXIN protein levels, decreased β-catenin protein levels, and decreased β-catenin/TCF4 transcriptional activity, which resulted in inactivating Wnt/β-catenin signaling and then downregulating the expression of Cyclin D, MMP-9, Snail, and MDR, which were closely associated with the development of ovarian cancer [23–26]. The gene discussed is TNKS; the disease is ovarian carcinoma.