The contribution of intracellular HSP90 to the development and maintenance of cancer stemness may be yet wider and deeper and include other HSP90-dependent mechanisms, for example, HSP90–telomerase (hTERT) interactions (it seems likely that they ensure endless mitoses of CSCs) or HSP90–immunophilin interactions (see [48,50], Figure 2, and further Section 3.6). This evidence concerns the gene HSP90AA1 and cancer.