Although the relationship between microbiota and metabolites in individuals with GC with H. pylori has not been thoroughly described, it is evident that the secondary metabolites produced by H. pylori elevate the metabolism of citric acid and carbohydrates in the gastric tissue of patients with GC (31), exacerbate inflammation in the gastric tissue by stimulating the activation of C-type lectin receptors (32), and inhibit the interferon-alpha (IFN-α) signaling pathway to evade the immune system (33). The gene discussed is CLEC4D; the disease is gastric cancer.