It has been known since long time that NF-κB is frequently activated in solid and blood cancer,2, 3 stemming the idea that its oncogenic function relays on inhibition of cancerous cell death, driven either by antitumor drugs or tumour-suppressor mechanism.3 This hypothesis, robustly based on experimental models, originated the valid assumption that inhibiting NF-κB activity should be an effective therapeutic tool alone or in combination with chemotherapy or radiation therapy. The gene discussed is NFKB1; the disease is hematopoietic and lymphoid system neoplasm.