It is likely that such a strong therapeutic effect of AIM against AKI was mainly achieved through the removal of tubular-obstructing dead cell debris using the AIM-KIM-1 axis, as the lethal AKI induced in KIM-1−/− mice by IR plus HS was not improved by rAIM administration as profoundly as in wild-type mice. This evidence concerns the gene HAVCR1 and acute kidney injury.