Key disruptions include elevated LDL and reduced HDL promoting extra-gastric diseases, enhanced glycolysis via pathways involving HKDC1, Lonp1, and PDK1/Akt fueling epithelial proliferation and EMT, exploitation of host lactate (mediated by genes like hp0140-0141) facilitating bacterial colonization and immune evasion, and amino acid imbalances (BCAA accumulation activating mTORC1, gGT depleting GSH) causing oxidative stress and immune tolerance. Here, AKT1 is linked to stomach disorder.