Skip to main contents
Recognition for the Ennoblement of the Human Sprit in Academics, The Arts, and Human Welfare

2022 Laureates

Introduction Video

  • Medicine
  • Seung K. Kim
    Professor, Stanford University
  • Education & Work Experience
    1963 Born in Seoul, Korea, 1985 A.B., Biochemical Sciences, Harvard college, USA, 1992 M.D., Stanford University, School of Medicine, USA, Ph.D., biochemistry, Stanford University, USA, 1998 Research Fellow, Harvard University, USA 1998~ Professor, Stanford University, School of Medicine, USA 2008~ Investigator, Howard Hughes Medical Institute, USA


Professor Seung K. Kim has made significant contributions to our understanding of the mechanisms of pancreas development and expansion of insulin-producing beta-cells. In seminal early studies, he revealed native signaling pathways crucial for early pancreas development, thus accelerating discoveries of important signaling factors currently used to generate replacement beta-cells from sources like embryonic stem cells. More recently, his group also developed methods to purify endogenous islet precursor cells from the pancreas, revealed their molecular profile, and established methods to differentiate these precursors into functional islet of Langerhans cells, including insulin-secreting beta-cells. Thus, his research findings established an important foundation for research by others, and will likely continue to have a long-lasting impact.
He also made significant contributions in our understanding of the regulatory mechanisms controlling beta-cell expansion. For treating diabetes mellitus, where the number or function of beta cells is lost, it is important to understand the mechanisms of beta-cell development and expansion. In studies published in Nature(in 2006), he demonstrated the crucial role of the Calcineurin/NFATc signaling pathway in beta-cell expansion, and revealed how human immunosuppresants like tacrolimus can cause diabetes mellitus. His group has also demonstrated how a cell cycle inhibitor called “menin” suppresses beta-cell expansion, findings relevant to beta-cell growth in multiple forms of diabetes. In recent work, including a 2011 study published in Nature, he discovered that PDGF receptor signaling in beta-cells declines with age, revealing how adult beta-cells naturally lose their capacity to expand in response to growth factors. Collectively, this work has identified new strategies for expansion of beta-cells, and further work is under way to convert these findings into therapeutic options for diabetes.