Given the association between NF-κB+ and key subtypes exhibiting poor overall survival (MAF, 1q gain), it is possible subtype-specific epigenomic backgrounds may be predisposing towards p52-driven oncogenic re-wiring events and therefore lead to preferential accumulation of activating mutations such as TRAF3 throughout the clonal evolution of MM tumours. Here, NFKB1 is linked to neoplasm.