For example, Li and others have shown that circ-ITCH shared the same miRNA binding sites with the 3’-untranslated region (3’-UTR) of the transcript from its host gene ITCH, and that circ-ITCH increased the expression of its host gene ITCH by sponging several miRNAs including miR-7, miR-17, and miR-214, thus inhibiting the Wnt/β-catenin pathway and the proliferation of esophageal squamous cell carcinoma cells and tumor growth in vivo by promoting ubiquitin-mediated Dvl2 degradation and decreasing the expression of oncogene c-Myc [26]. The gene discussed is ITCH; the disease is neoplasm.