In summary, our data demonstrated for the first time that abnormally activated Wnt/β-catenin/TCF3 signaling in GC cells, which cooperated with HOXA11-AS and miR-17-5p, promoted the downregulation of ATF3, which in turn elevated the expression of β-catenin and CEMIP and further enhanced the imbalanced Wnt/β-catenin signaling, synergistically accelerating the development of GC (Fig. 7l). The gene discussed is HOXA11; the disease is gastric cancer.