The overactivation of AKT/mTOR, a downstream signaling pathway of JAK, leads to interstitial fibrosis, and treatment with ruxolitinib effectively reduces the inflammation and oxidative stress induced by unilateral ureteral obstruction (UUO), probably because ruxolitinib reduces the activity of the AKT/mTOR pathway and reduces SASP damage to renal tubular epithelial cells [142]. The gene discussed is AKT1; the disease is Ureteral obstruction.