NFKB1 and neoplasm: A biphasic ROS response emerges: Subtoxic levels activate proto-oncogenic signaling pathways (e.g., NF-κB, AP-1) to drive tumor progression; Supraphysiological accumulation causes oxidative DNA damage-induced genomic instability and initiates programmed cell death pathways, including apoptosis, ferroptosis, and disulfidptosis.