Excessive parietal cell apoptosis driven by ER stress and impaired autophagy culminates in hypochlorhydria and intrinsic factor deficiency, the basis of pernicious anemia, whereas persistent activation of ERK/MAPK, PI3K/Akt, and STAT3 sustains ECL cell proliferation and survival, fostering progression toward type 1 gNENs. This evidence concerns the gene AKT1 and pernicious anemia.