We did not find significant changes of p53 in the cytosolic fraction after HI, which is different from previous reports that showed an increase in cytosolic p53 in neonatal rats after HI47 and a decrease in adult rats after cerebral ischemia.48 The discrepancy between these reports suggests that p53 translocation between the cellular compartments is age, species, and injury dependent and might be related to different cell death mechanisms. The gene discussed is TP53; the disease is brain ischemia.