In this study, we showed that the oral application of a drug that preferentially targets JAK1 and JAK3, TOFA, had beneficial effects in LPS-induced AKI mice as indicated by (a) a significant amelioration of BUN and Scr elevation, renal histological changes, and oxidative stress dysregulation, and (b) suppression of the production of proinflammatory cytokines and the activation of downstream signaling pathways. The gene discussed is JAK3; the disease is acute kidney injury.