In contrast, it is largely unknown whether and how cancer cells can also escape the effects of HSP90 blockade; however, the preclinical observation that cultured glioblastoma cells developed tanespimycin resistance due to reduced expression of the NAD(P)H dehydrogenase quinone 1, a cellular enzyme responsible for modifying tanespimycin for increased binding to HSP90 [22], indicates that clinical resistance will occur as more patients are being treated with these agents. This evidence concerns the gene HSP90AA1 and glioblastoma.