The present work demonstrated that DEK depletion was accompanied by increased protein stability and transcriptional activity of the p53 tumor suppressor, and subsequent upregulation of pro-apoptotic proteins, such as Bax, which promotes the release of cytochrome c from the mitochondria (caspase-3 and −9 increased), initiating the apoptotic cascade (Fig. 9). The gene discussed is CYCS; the disease is neoplasm.