DNA replication stress is observed during tumor initiation, and the induction of such stress in AEG-1 knocked-down cells significantly reduced the half-life of SND1 protein, and, conversely, AEG-1 overexpression increased SND1 protein stabilization upon heat shock, suggesting that AEG-1/SND1 interaction aids in cell survival under stressful conditions [75,108]. The gene discussed is SND1; the disease is neoplasm.