Among anti-chemotherapy or radio-resistant process ofglioma cell lines, autophagy plays an important role in regulating cell responses to cell stress.It is an evolutionarily conserved degradative process initiated by autophagosomes, a double-membrane structure that sequester cytoplasmic material and fuse with endosomes and lysosomes to become autolysosomes.Multiple cellular stressors, including activation of the tumor suppressorp53, can stimulate autophagy.p53 mutates in a high percentage of human tumors.However, many other tumors retain wild-type (wt)p53 expression, raising the intriguing possibility that they actually benefit from it.Recent studies imply a role forp53 in regulation of autophagy, a catabolic pathway by which eukaryotic cells degrade and recycle macromolecules and organelles, particularly under conditions of nutrient deprivation.P53 protein, influencing autophagy by mARF.DRAM, P21, BCL2 family members, and so on, promotes autophagy cell death or protects cell from apoptosis, a process of caspaseindependent cell death.Researchers found that TNF family mainly promotes cell apoptosis, necrosis and autophagy cell death in nervous system.P53 regulates TNF family pathway under autophagy and influences the sensitive to TNF-α.In contrast to WT-p53 cell line, P53 mutation protects it from cell death under autophagy.Our aim is to enhance glioma cell line cell death by changing P53 gene under autophagy.