Accumulating evidence revealed that ASK1 activation accelerates renal injury through the activation of p38 and JNK cascades in rodent models of kidney injury, including ischemia/reperfusion-induced AKI, unilateral ureteric obstruction, and diabetic nephropathy [45,46,47], and that treatment with GS-444217, an inhibitor of ASK1, limited the loss of podocytes most likely through the anti-apoptosis pathway in a diabetic kidney disease mouse model, indicating ASK1 as an important target for podocyte injury [48]. Here, MAP3K5 is linked to acute kidney injury.