During the development of H. pylori-induced CG into early gastric cancer, Lewis antigens of H. pylori LPS could interact with Mincle (Macrophage inducible C-type lectin) and maintain a balance between pro- and anti-inflammatory cytokine production, suggesting that the C-type lectin receptor signalling pathway is closely related to the mechanism employed by H. pylori to escape the host innate immune receptors [43]. Here, CLEC4E is linked to gastric cancer.