While multiple control mechanisms normally ensure the prompt cessation of physiological NF-κB signalling, in most human cancers, numerous alterations constitutively activate NF-κB, enabling it to fuel tumour progression, metastatic dissemination and therapy resistance by regulating genes that suppress cancer-cell apoptosis and orchestrate inflammation in the tumour microenvironment (TME), thus hijacking the ancient connection between apoptotic and inflammatory pathways [2, 3]. Here, NFKB1 is linked to neoplasm.