Its core mechanism involves the bidirectional regulation of cellular signaling networks: on one hand, it inhibits pro-tumorigenic signals such as Akt/mTOR, NF-κB, Wnt/β-catenin, and STAT3, thereby blocking tumor proliferation, invasion, and metastasis; on the other hand, it activates tumor-suppressive and cytoprotective pathways, including AMPK, p53, and nuclear factor erythroid 2-related factor 2 (Nrf2), which induce cell cycle arrest and apoptosis [7,8]. This evidence concerns the gene AKT1 and neoplasm.