Several Hsp90–Cdc37 disruptors, including DCZ3112 and platycodin D, have been shown to suppress AKT phosphorylation, thereby dampening prosurvival signaling and sensitizing cancer cells to apoptotic cues.44,57 In parallel, inhibition of the ERK/MAPK pathway has been observed with compounds such as DCZ3112 and okicamelliaside, both of which markedly reduce ERK1/2 phosphorylation, impairing cell proliferation and migratory potential.37,57 A notable therapeutic advantage of targeting the Hsp90–Cdc37 complex is the ability to interfere with adaptive resistance mechanisms. The gene discussed is AKT1; the disease is cancer.