As to the role of autophagy in the I/R-injured neurons, we believe that its significance is considerable and nonnegligible, based on the following evidence: (1) after stroke models were built either in vivo or vitro, the level of autophagy related protein (LC3-II, by western blotting) was altered, which was reversed by knockout of p53, and knockdown of PRAS40 at least partially abolished this effect; (2) immune-fluorescence assay not only revealed the protein level alteration of LC3-II but also the formation of the autophagosome. Here, TP53 is linked to stroke disorder.