JNK activation has been detected in many forms of kidney disease [22] In animal models, JNK inhibition prior to ischemia-reperfusion or tubule obstruction reduces inflammation and fibrosis, and preserves kidney function [23–27] Interestingly, acute kidney injury exacerbates polycystic kidney disease [28–30] In chronic kidney insult, progressive interstitial fibrosis contributes to organ failure. This evidence concerns the gene MAPK8 and kidney disorder.