EGFR and acute kidney injury: In an ischemic/reperfusion (I/R)-induced mice model, we also showed that severe I/R injury induced a sustained activation of EGFR, which is required for renal regenerative responses (tubular cell dedifferentiation and proliferation) in the early phase, but is, in turn, a critical mediator of renal fibrogenesis in the later phase of acute kidney injury (AKI) [66].