Clinico-pathological observations strongly indicated proinflammatory actions of the CagA protein in gastric pathogenesis and CagA contributes to a pro-inflammatory microenvironment associated with the development of chronic gastritis through the activation of NF-κB pathway.11,54 In line with this, we also noted a positive correlation between the intensity of AUF1 expression, CagA level in gastric juices exosomes and the severity of inflammation in H. pylori-infected gastric mucosal tissues from patients (Figure 6). The gene discussed is NFKB1; the disease is chronic gastritis.