Some evidence suggests that p53 activates the p65 subunit of NF-κB via the ribosomal S6 kinase 1 [18] and TNF triggers a transcriptionally active complex of p65 and p53 on κB response elements, indicating that mutated p53 rather than loss of p53 contributes to tumor progression [19]. The gene discussed is RPS6KA1; the disease is neoplasm.