Davies’ research centers on the role of free radicals and oxidative stress in biology for which he coined the term, “The Oxygen Paradox.” In particular he is interested in genes that repair oxidatively damaged proteins, lipids, RNA, and DNA, and his laboratory has made major contributions to our understanding of this subject over the past thirty years. Davies discovered key roles free radicals play in exercise, and in mitochondrial redox-cycling-dependent cardiotoxicity of the chemotherapy drug Adriamycin. He uncovered stress-protection by Proteasome and the Lon protease, and discovered several stress-related genes, including RCAN1 which contributes to Alzheimer’s disease, Down syndrome, and Huntington’s disease. Davies demonstrated that impaired induction of the Proteasome and of the mitochondrial Lon protease genes contributes to senescence and severely diminished stress-resistance in aging. He developed the concept of Adaptive Homeostasis and has demonstrated the significance of its decline in both aging and chronic diseases.