This review introduces the mechanism underlying RCC metastasis to the stomach, integrating PI3K/AKT-driven survival, Ras/MAPK-mediated motility, and Wnt-orchestrated metabolic plasticity with concurrent angiogenic reprogramming, extracellular-matrix remodeling, and exosome-mediated signaling. The gene discussed is AKT1; the disease is renal cell adenocarcinoma.