The mTOR pathway is activated by multiple growth factor receptors, namely, epidermal growth factor receptor (EGFR), Human Epidermal growth factor Receptor 2 (HER2), insulin-like growth factor type 1 receptor (IGF-1R), that are overexpressed in many gastric tumors.[26, 27] mTOR regulates production of angiogenic factors (VEGF/VEGFR) that promote new vessel formation and predict poor outcome in patients with gastric cancer.[28] mTOR regulates nutrient uptake and cell metabolism and contributes to the characteristic metabolic changes in cancer. Here, ERBB2 is linked to gastric neoplasm.