We show that MYC and/or IL-6-driven B cell and plasma cell tumors of mice exhibit constitutive NF-κB activity that leads to overexpression of NF-κB target genes such as Cdkn1a and Fancd2. These genes encode the well-established tumor suppressor, p21, and a key member of the Fanconi anemia/breast cancer DNA damage repair pathway, respectively. This evidence concerns the gene NFKB1 and neoplasm.