In light of the variety of genetic lesions in lymphoid malignancies which can cause constitutive NF-κB activation through deregulation of distinct upstream signaling nodes, the ultimate goal in the treatment of cancer, i.e., the highly specific eradication of the tumor cells by a targeted therapy, requires the analysis of the relevant oncogenic lesions and deregulated signaling pathways in the respective lymphoid tumor. The gene discussed is NFKB1; the disease is neoplasm.