mTOR is an important metabolism-regulating protein kianse. Although its main role is to regulate protein synthesis and cell growth, it also has a profound effect on cellular redox homeostasis. It can control expression and activities of important redox enzymes, and at the same time, it controls autophagy, which eliminates reactive oxygen species (ROS)-producing dysfunctional mitochondria. Tissues with mTORC1 hyperactivation often experiences elevated oxidative stress which can damage the cell and tissues and interfere with diverse physiological processes. This can explain how aberrant mTORC1 activation in diverse tissues can induce pathological features that are associated with oxidative damage but often unrelated to cell growth. We will approach the relationship between mTOR and redox signaling pathways through combining structural, genetic, cell biological and proteomic approaches.