AKT1 and gastric cancer: For example, Helicobacter pylori‐induced activation of EGFR‐PI3K/Akt signaling resulted in GSK3β suppression and β‐catenin accumulation through VacA or OipA.36, 37, 38 We previously reported that M hyorhinis infection activated the EGFR‐PI3K/Akt signaling axis in gastric cancer cell lines.5 Therefore, it will be interesting to examine the association between the β‐catenin pathway and the EGFR‐PI3K/Akt pathway.