Under the condition of chronic stimulation by H. pylori lysates, VacA and CagA delivered to host cells via outer membrane vesicles (OMVs) upregulated the expression levels of NOD1 and RIP2, and inhibited GC cell apoptosis and autophagy through the MAPK-ERK/Forkhead box subclass O protein 4 (FOXO4) pathway, ultimately inducing bacterial immune escape, tumor cell invasion and metastasis, and EMT (He et al., 2020). This evidence concerns the gene MAPK1 and gastric cancer.