Beth Levine receives the 2014 ASCI/Stanley J. Korsmeyer Award.

Autophagy is an evolutionarily conserved process that degrades large cellular components and plays a critical role in maintaining cellular homeostasis. This year, the ASCI recognizes seminal work in the field by Beth Levine (Figure 1) of the University of Texas Southwestern Medical Center with its annual Stanley J. Korsmeyer Award. The prize honors Levine for her groundbreaking studies that first elucidated the genetic control of autophagy in mammalian systems and subsequent work that has implicated the autophagy pathway in the pathogenesis of a wide spectrum of diseases, including cancer, aging, neurodegeneration, infectious diseases, and diabetes. Levine recently talked with the JCI to discuss her extraordinary path in research. JCI: What first attracted you to a career in medicine and then in research? Levine: I was originally attracted to a career in medicine for what I think is a typical reason: I wanted to help people. I found clinical medicine very gratifying from a personal and humanistic point of view. I loved clinical medicine, but I loved research even more. Research provided more opportunities for intellectual creativity and discovery and more opportunities to have a long-term impact on human disease. When you are caring for an individual patient, it is intellectually stimulating to try to understand what is going on and personally gratifying if you can use this understanding to help the patient. But you are only filling in the pieces of a small puzzle. There is no room for generating testable hypotheses to solve bigger puzzles in biology and medicine, which can potentially allow you to have a greater impact on more people. JCI: Your early research focused on infectious diseases and viral pathogens. How did this line of study lead you to autophagy? Levine: This actually ties to Stan Korsmeyer himself and his work on apoptosis. When I was a fellow, he was in the early days of his pioneering work on the role of BCL2 in the regulation of apoptosis and lymphoma. When I was a postdoctoral fellow, it occurred to me that we really did not know how viruses kill cells and why certain cells were resistant to lytic viral replication. So, using Sindbis virus, an alphavirus that provides an animal model for studying human arthropod-borne encephalitides, I showed that Sindbis virus killed cells by inducing apoptosis, that BCL2 blocked the process, and that BCL2 overexpression protected mice against lethal viral encephalitis. While