Downstream, K63-Ub/SQSTM1 accumulation results in the sequestration of damaged mitochondria, the CYLD K63 DUB, and the activation of the K63-Ub TRAF6-NF-κB pathway, providing metabolic, survival, inflammatory, and proliferative advantages to tumor cells (Figure 1). The gene discussed is NFKB1; the disease is neoplasm.