Ischemia/reperfusion injury (IRI) is an important component of organ dysfunction after transplantation. One of the consequences of IRI is activation of the innate immune response. Danger signals released by the damaged cells interact with membrane receptors to ultimately enhance the inflammatory response. Dr. Bonventre will discuss the role of KIM-1/TIM-1 on epithelial cells in down-regulating the innate immune response through NF-kB, and increasing autophagy and pro-tolerogenic MHC expression in the early phases of injury. Often IRI and associated acute kidney injury leads to chronic kidney disease. Prolonged expression of KIM-1/TIM-1 leads to a maladaptive response resulting in persistent tubular injury and a senescent secretory profibrotic phenotype.