Tumor microenvironment-derived ROS, generated through mitochondrial dysfunction, TLR activation, or intratumoral microorganisms, activates redox-sensitive NF-κB/AP-1 pathways in cancer cells and TAMs, leading to chronic inflammation via inflammatory cytokine release (Glorieux et al., 2024) (Figure 2C). Here, NFKB1 is linked to neoplasm.