The results demonstrated that 17-DMAG or Hsp90β knockdown effectively reduced the interactions of TAK1 (TGF-β-Activated Kinase 1), AMPKα, IKKα/β, HIF-1α and Raptor (regulatory-associated protein of TOR, an important positive regulatory subunit of mTOR complex) with Hsp90β, indicating that endogenous Hsp90β protein complex was required to maintain the high-salt-diet-induced nephropathy. The gene discussed is HIF1A; the disease is kidney disorder.