It is generally thought that, as a bacterial oncoprotein, CagA plays a key role in H. pylori-induced gastric cancer [5, 6] as it affects the expression and function of key proteins involved in oncogenic or tumour suppressor signalling pathways via several molecular mechanisms such as direct binding or interaction, phosphorylation of vital signalling proteins, and methylation of tumour suppressor proteins [7, 8]. This evidence concerns the gene S100A8 and gastric cancer.