Pharmacological inhibition of the N-terminal ATP-binding pocket halts the Hsp90 chaperone cycle [5]; however, first-generation N-terminal Hsp90 inhibitors have shown limited clinical efficacy in breast cancer and frequently trigger an HSFthera1-mediated heat shock response (HSR), which upregulates Hsp70 and other chaperones, thereby weakening antitumor activity and contributing to toxicity [6,7]. This evidence concerns the gene HSP90AA1 and breast carcinoma.