I became interested in science because of a fascination with the process of biological aging. My initial scientific training was in basic biochemistry, specifically as it pertains to mitochondrial reactive oxygen species and their role in the pathogenesis of aging and age-related diseases. The highlight of my work was the finding that the Qo site of Complex III can release superoxide to both sides of the inner mitochondrial membrane, ultimately causing molecular damage in both the cytosol and the mitochondria. During my post-doc in the lab of Ron DePinho at the Dana-Farber Cancer Institute, I studied the role of Foxo transcription factors in aging and neurodegeneration. However, during this time, I decided to change the focus of my work to cancer: I felt (and still feel) that the field of biological aging is deficient with regards to independent validation of critical findings, especially lifespan studies in mice. At the same time, seeing cancer patients every day whilst working at DFCI, led me to focus on research with more immediate applicability. As such, I applied my knowledge in basic biochemistry and metabolism, to the nascent field of oncogenomics, the study of genetic alterations of cancer. The key observation driving my current work, was the finding that genomic deletions in cancer frequently inactivate not only tumor suppressor genes (which gives a fitness advantage) but also nearby chromosomal neighbors, many of which play critical but redundant roles in housekeeping metabolic functions. This co-deletion of such metabolic genes is fitness neutral but can cause specific metabolic vulnerabilities that may be exploited by specific drugs. The goal of our lab is to identify such metabolic vulnerabilities exposed by genomic deletions and devise molecular targeted therapeutics to exploit these.​