The article reviews the interaction between reactive oxygen species (ROS) and the transcription factor NF-κB, which plays a crucial role in inflammation, immunity, and various cellular processes. ROS are produced by various cellular processes and can act as both stimulators and inhibitors of NF-κB signaling. The regulation of ROS levels by NF-κB targets and the impact of ROS on NF-κB signaling pathways are discussed. Key NF-κB targets that influence ROS levels include manganese superoxide dismutase (MnSOD), copper-zinc superoxide dismutase (CuZn-SOD), ferritin heavy chain (FHC), thioredoxin-1 (Trx1), and glutathione peroxidase-1 (Gpx1). These proteins protect cells from oxidative damage. On the other hand, some enzymes that promote ROS production, such as NADPH oxidases, xanthine oxidase, and nitric oxide synthases, are also regulated by NF-κB. The article highlights the complex and context-dependent interactions between ROS and NF-κB, emphasizing the importance of ROS in modulating NF-κB activity and vice versa.The article reviews the interaction between reactive oxygen species (ROS) and the transcription factor NF-κB, which plays a crucial role in inflammation, immunity, and various cellular processes. ROS are produced by various cellular processes and can act as both stimulators and inhibitors of NF-κB signaling. The regulation of ROS levels by NF-κB targets and the impact of ROS on NF-κB signaling pathways are discussed. Key NF-κB targets that influence ROS levels include manganese superoxide dismutase (MnSOD), copper-zinc superoxide dismutase (CuZn-SOD), ferritin heavy chain (FHC), thioredoxin-1 (Trx1), and glutathione peroxidase-1 (Gpx1). These proteins protect cells from oxidative damage. On the other hand, some enzymes that promote ROS production, such as NADPH oxidases, xanthine oxidase, and nitric oxide synthases, are also regulated by NF-κB. The article highlights the complex and context-dependent interactions between ROS and NF-κB, emphasizing the importance of ROS in modulating NF-κB activity and vice versa.