On one hand, based on the in vitro and mouse model research, studies have elucidated that Hp dwelling exerts the reduction of MUC1 expression due to the mucosal barrier injury [9–11], whereas, on the other hand, it was suggested that glycan-rich niche produced by mucins provides a preferential binding point for Hp [9]; notably, the abnormal expression of MUC1 was recognized as oncogene in the development of gastric carcinomas [12, 13]. The gene discussed is MUC1; the disease is gastric carcinoma.