Notably, compared to the patients with gastritis, the levels of ANGPTL4 in the patients with gastric ulcer were significantly higher (Fig. 7J), along with the down-regulation of tight junction protein CLDN1 by ANGPTL4 (Figs. 4 and 5) and the decreased transepithelial electrical resistance (TEER) values in ANGPTL4-stimulated AGS cells (Fig. S16F), suggesting potential roles of H. pylori-induced ANGPTL4 in the damage of gastric mucosa. This evidence concerns the gene CLDN1 and gastritis.