An additional argument in favor of this scheme is an experimentally established fact that the genetically determined decomposition of a KEAP1/CUL3/RBX1 complex with an E3-ubiquitin ligase that regulates both NRF2 and NF-κB signaling pathways appeared to be the key mechanism triggering NF-κB activation in human lung cancer cells [72]. The gene discussed is NFKB1; the disease is lung cancer.