Genetic amplification of NF-κB signaling—through constitutive IKKβ activation or deletion of ubiquitin-modifying enzyme A20 (TNFAIP3)—enhances tumor-specific IFN-γ production, augments cytotoxic function, and promotes tumor rejection in preclinical models [319–321]. The gene discussed is NFKB1; the disease is neoplasm.