Increased ROS generation uniquely sensitizes oncogenically transformed and cancer cells, but not non transformed cells, to cell death, indicating that neoplastic cells are far more at risk of increased intracellular oxidative stress. diminution in mTOR signaling appears to be the main underlying mechanism. It’s known MAP kinase inhibitor that malignant lymphoma, a heterogeneous disease with very variable clinical course and prognosis, could be the most prevalent kind of adult leukemia. Most people with MLs in clinical course are hostile and soon after diagnosis require intensive treatment. The balance between pro and anti apoptotic molecules, and aberrant up-regulation of prosurvival mechanism have now been proven to be related to resistance of ML cells to radiation therapy and chemotherapy. Previous clinical studies have demonstrated that symptomatic ML can be effortlessly treated with purine analogs, glucocorticoids, alkylating agents or monoclonal antibodies. Nevertheless, some patients with relapsed or refractory infection have limited therapeutic options. Consequently, there’s an urgent need to discover more efficient and less toxic drugs for ML patients. Inhibitors Cellular differentiation of 3 hydroxy 3 methyl glutaryl coenzyme A reductase are used to treat hypercholesterolemia. Convincing evidence from both in vitro and in vivo data has demonstrated that statins exert pleiotropic actions beyond their lipid-lowering consequences, including cancer prevention and immune regulation. Statins have now been proven to cause cell death and cell cycle arrest in a variety of cancer cells for example pancreatic cancer cells, multiple myeloma cells, non-small lung cancer cells, waldenstrom macroglobulinemia cells, glioblastoma cell lines and HT29 cells. A current study indicates HCV NS3 protease inhibitor that simvastatin inhibits proliferation of MCF 7 cells in parallel with an increase in reactive oxygen species production. Another lipophilic statin, atorvastatin, has also been proven to raise levels of myocardial protein oxidation and lipid peroxidation. Furthermore, a higher dose of atorvastatin induces oxidative DNA damage in human peripheral blood lymphocytes. Previous studies have demonstrated that cancer cells produce higher levels of ROS than normal cells and this contributes to cancer development. To keep ROS at physiological levels, cancer cells possess an antioxidant defense system which includes glutathione and glutathione dependent enzymes such as superoxide dismutase and catalase to get rid of ROS. Given these previous findings, we hypothesized that statins use at least some of their cytotoxic outcomes by increasing oxidative stress based on cell type. In our study, we examined the ramifications of statins including simvastatin, fluvastatin and atorvastatin on survival of lymphoma cells such as A20 and El4 cells, and explored the potential underlying mechanism.