HIF1A and neoplasm: Paradoxically, tumor-derived ROS subvert this process through dual mechanisms: (1) the stress-induced downregulation of NKG2D ligands via HIF-1α-dependent transcriptional suppression [33]; (2) mitochondrial permeability transition pore (mPTP) activation through cyclophilin D oxidation, triggering caspase-3-mediated apoptosis [34].