NFKB1 and cancer: These were related to activation of stress responses (hypoxia, UV and UPR), immunity (inflammation, interferon gamma response, TNF-α activation via NFκB, complement, and IL2/STAT5 signaling), metabolism (cholesterol homeostasis, adipogenesis, metabolism of heme and xenobiotics, and androgen and estrogen early and late responses), fibrosis (mTORC1 and TGF-β), cell adhesion disruption (apical junction), protein secretion, coagulation, and other processes typically altered in cancer, such as apoptosis (p53 pathway) and proliferation and survival (p53 pathway) (Figs. 3 and 4).