In tumor entities where the activity of both the canonical and alternative NF-κB pathways has been implicated in the pathogenesis (e.g., HL, MM) (Table 1), it will be important to identify the individual contributions of either pathway, and to determine the extent to which the functional ablation of the separate pathways affects tumor cell growth or survival. The gene discussed is NFKB1; the disease is Miyoshi myopathy.