Interestingly, EPHA2-silencing in the context of infection alters the expression of some angiogenic-related factors to levels that are lower (fold-change of ≤0.5) or higher (fold-change of ≥1.5) than those of siEPHA2 silencing in the uninfected setting (siEPHA2_U), thereby pointing to its involvement in crosstalk with other angiogenic-regulating genes triggered by H. pylori infection (Table 2). This evidence concerns the gene EPHA2 and infection.