Figure 2: NF-κB signaling pathway, inflammation, and carcinogenesis induced ROS. Excessive reactive oxygen species (ROS) derived from mitochondrial membrane, xenobiotics, and enzyme reactions activate IKK. Activated IKK phosphorylates IκB and leads to ubiquitination and proteasome degradation of IκB, releasing NF-κB proteins, such as p50 and p65. The free p50 and p65 translocate into nuclei and drive target gene expression, such as inflammatory cytokines, leading to inflammatory lesions and carcinogenesis.