AKT1 and cancer: In agreement with their activity as Hsp90/Cdc37 interface inhibitors, both of our novel inhibitors dose-dependently decreased the expression of established Hsp90 clients (C-Raf, Akt, ERK), while not inducing the expression of Hsp90 or Hsp70 in the four cancer cell lines, unlike 17-AAG (Figure 6A–D).