An increase in the neuronal “prone to die” state, promoting Alzheimer’s disease in DS, may be due in part to altered levels of anti-apoptotic proteins: Bax apoptosis-activating proteins were elevated and anti-apoptotic Bcl-2, heat shock protein 70, neuronal apoptosis inhibitory protein and p53 were decreased [67]. The gene discussed is TP53; the disease is Alzheimer disease.