Although mouse gastric cancer cells stably expressing CLDN18-ARHGAP26 did not significantly differ from empty vector-expressing cells in proliferation, epithelial-mesenchymal transition, tumorigenicity, and sphere-forming capacity (Supplementary Figs.10‒14), migration ability was significantly enhanced following CLDN18-ARHGAP26 overexpression (Fig. 5a and Supplementary Fig. 15a; P < 0.001, Wilcoxon signed rank test). This evidence concerns the gene ARHGAP26 and gastric cancer.