In this regard, modulation of the HSP level in the body using both various physical factors (for example, hyperthermia) and chemical molecules (either inducers or inhibitors) should be based on the contribution of chaperones to the pathogenesis of the disease: presumably, for neurodegenerative diseases, an approach based on a compensatory increase in HSP can be an optimal tactic, while suppression of HSP in oncological diseases should take place. This evidence concerns the gene HSP90B2P and neurodegenerative disease.