In cancer, GABPA expression and activity are modulated by pathways such as PI3K/AKT/mTOR and AMPK that control tumor growth and metabolism; overexpression supports tumor proliferation and angiogenesis by enhancing energy production, while epigenetic silencing impairs mitochondrial gene activation, reducing tumor adaptability to hypoxia and shifting metabolism towards HIF-1α-driven glycolysis [148]. The gene discussed is GABPA; the disease is neoplasm.