However, EBV co-infection results in methylation of the host SHP 1 and keeps Cag A phosphorylation and thus may increase the oncogenic potential of Cag A. Fekadu et al. 36 found that H. pylori was exposed to the principal EBV receptor, CD21, in negative gastric epithelial cells, which could induce the expression of EBV receptors EphA2 and NMHC-IIA, and promote the EBV infection. This evidence concerns the gene MYH9 and Epstein-Barr virus infection.