A key therapeutic advantage of targeting the Hsp90–Cdc37 interface is the minimal induction of the heat shock response (HSR), which contrasts sharply with the effects of classical Hsp90 ATPase inhibitors.1,17 Traditional agents such as geldanamycin strongly upregulate Hsp70 and Hsp27, activating cytoprotective pathways that can promote tumor cell survival and contribute to treatment resistance.74 In contrast, compounds that disrupt the Hsp90–Cdc37 interaction tend to spare or only modestly activate this stress response. The gene discussed is CDC37; the disease is neoplasm.