HIF1A and neoplasm: Cytoprotective adaptations in HCC involve immune synapse destabilization through actin cytoskeletal remodeling[48], JAK-STAT hyperactivation, which confers resistance to IFN-γ-mediated apoptosis[49], and hypoxia-driven autophagy (HIF-1α-dependent), which degrades tumor antigens while expanding Tregs/MDSCs to sustain immunosuppressive niches[50].