That was likely the reason for Neckers and Workman5 to suggest stratification of cancer patients based on Hsp90 expression and oncogenic clients in the tumor cells prior to clinical trials. In brief, (1) the wide range of Hsp90 expression in normal organs and (2) the heterogeneous responses of tumors from different patients to the same inhibitor could have been a real cause for the failures of previous clinical trials. This evidence concerns the gene HSP90AB1 and neoplasm.