ESR1 and neoplasm: The rapid downregulation of p-PI3K and p-AKT at 6 h disrupts a key pathway driving high-risk NPC progression (Wang S. et al., 2021; Zhao et al., 2016), while the progressive inhibition of downstream effectors (AKT1, MTOR, HIF1A, SRC, ESR1) amplifies this anti-tumor effect by interfering with metabolic adaptation, hypoxia signaling, and growth factor receptor cascades (Cai et al., 2019; Liu et al., 2024c; Li H. L. et al., 2022).