Even in p53-deficient tumor cells, the fungal metabolite gliotoxin inhibited NF-κB activation with high selectivity, activated c-Jun N-terminal kinase (JNK), released cytochrome c from mitochondria, and potently stimulated the caspase cascade, inducing the cleavage of caspase-9, -8, -7, and -3 [46]. The gene discussed is TP53; the disease is neoplasm.