CD274 and neoplasm: In pathological contexts, chronic ROS accumulation subverts this balance through dual mechanisms: (1) sustained oxidation inactivates IκB kinase, blunting NF-κB-dependent survival signals and cytokine production [29,30]; (2) ROS-mediated post-translational modifications stabilize PD-L1 on tumor cells, creating immune-evasive niches [8,9].