NFKB1 and neoplasm: On the one hand, ROS can activate a variety of redox reactions and signaling pathways, such as the MAPK pathway, PI3K/AKT pathway, NF-κB pathway, and Keap1-Nrf2-ARE pathway, to promote tumor occurrence, development, and metastasis; on the other hand, when ROS exists in excess, it can cause cellular stress and damage through oxidative stress mechanism and eventually lead to cell death [62–64].