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Nancy Andrews was Dean of the School of Medicine at Duke University from 2007-2017 and continues on the faculty. Previously she was at Harvard Medical School and Boston Childrenā€™s Hospital, where she was an investigator of the Howard Hughes Medical Institute. Her laboratory discovered molecules important in mammalian iron homeostasis and worked out the molecular causes of several diseases characterized by abnormal iron handling. In addition to the NAS, Andrews is an elected member of the NAM and the American Academy of Arts and Sciences.

She is a past president of the American Society of Clinical Investigation, and past Chair of the Board of the Burroughs Wellcome Fund. She currently serves as Chair of the Board of the American Academy of Arts and Sciences and as a member of the Boards of Directors of Novartis, Charles River Laboratories and Maze Therapeutics. She is a member of the Scientific Advisory Board for Dyne Therapeutics.

Andrews also serves on the Executive Committee of the M.I.T. Corporation. Andrews received her B.S. and M.S. from Yale, her Ph.D. from M.I.T., and her M.D. from Harvard Medical School. She did her clinical training at Boston Childrenā€™s Hospital and Dana-Farber Cancer Institute.

Nancy Andrews' laboratory is interested in mammalian iron homeostasis and its disruption in human diseases. Through positional cloning of the affected genes in classical rodent mutants with anemia, her group identified the first mammalian transmembrane iron transporter and demonstrated its importance in intestinal iron absorption and red blood cell differentiation. They characterized a second transmembrane iron transporter that releases iron from cells and showed that insufficiency of a peptide that regulates that transporter is fundamentally important in the pathogenesis of hemochromatosis, an iron overload disorder. They proposed that diminished cellular iron export plays a major role in the anemia of inflammation and, with others, confirmed that hypothesis. Starting with a patient that Andrews treated, her group identified the gene responsible for a disorder that they named iron-refractory iron deficiency (IRIDA). Recently, the Andrews lab has determined new roles for the classical transferrin receptor, suggesting that iron and the transferrin receptor may have relevance to a variety of diseases that have not generally been considered iron disorders.