Extrapolating the findings that canonical and alternative NF-κB subunits have distinct functions in the various B-cell subsets which represent the normal counterparts of lymphoid malignancies, identifying the roles of the individual oncogenic NF-κB transcription factors in these tumor subtypes may be exploited for the development of more specific therapies that target aberrant NF-κB activity. This evidence concerns the gene NFKB1 and neoplasm.