In this context, one can state that H. pylori plays an essential role in gastric carcinogenesis by establishing a chronic inflammatory state, activating oncogenic signaling pathways (e.g., STAT3, ERK, PI3K/Akt), promoting extracellular matrix remodeling and angiogenesis, and inducing epigenetic changes that inhibit tumor suppressor mechanisms. This evidence concerns the gene AKT1 and neoplasm.