Dr. Hato is Associate Professor of Medicine and Adjunct Associate Professor of Medical & Molecular Genetics at Indiana University School of Medicine and the Indianapolis VA Medical Center. He gained extensive clinical experience before joining the faculty in the Division of Nephrology at Indiana University. He obtained his MD in Japan and completed his residency and nephrology training both in Japan and the United States. He then worked as a full-time hospitalist and clinical educator for an additional four years before joining the faculty. Dr. Hato’s research focuses on elucidating the cellular and molecular mechanisms of sepsis-associated acute kidney injury, the most common kidney problem encountered in hospital settings. Regardless of the specific initiating pathogen, the clinical manifestations of septic kidney injury are largely indistinguishable, and histopathological examination offers only nonspecific findings. Because the current immunological paradigm does not fully explain the basis of sepsis-associated kidney injury, he proposes an alternative, unifying hypothesis that pathogen-induced inflammatory responses culminate in self-RNA overburden, leading to host translation shutdown. Importantly, this shutdown phase also represents a crucial transition period where tissue recovery begins. His group identified that bacterial sepsis triggers profound antiviral responses in the kidney due to the induction of endogenous double-stranded RNA. This double-stranded RNA stress not only causes translation shutdown but also initiates subsequent endogenous recovery programs by activating adenosine-to-inosine RNA editing in key anabolic genes, such as the enhancer of polyamine biosynthesis, antizyme inhibitor 1. Collectively, these findings suggest a general model in which inflammation and resultant RNA editing function as a rational auto-regulatory system, safeguarding against sustained metabolic shutdown and providing cues for tissue recovery.