Moreover, as a tumor-suppressive gene, CYLD deletion and mutation have been observed in 17% and 2.4% of MM patients[23] in association with aggressive disease through NF-κB and Wnt/β-catenin signaling regulation.[23,28–30] All these genetic abnormalities might result in a high-risk state and cause drug resistance. The gene discussed is NFKB1; the disease is neoplasm.