In response to ischemia- and cisplatin-induced AKI, the anti-inflammatory effect of KIM-1 expression is due to the interaction of KIM-1 with p85 and subsequent PI3K-dependent downmodulation of NFκB, suggesting that KIM-1-mediated epithelial cell phagocytosis of apoptotic cells may protect the kidneys after acute injury by downregulating NFκB (94). The gene discussed is HAVCR1; the disease is acute kidney injury.