Presumably, low anti-cancer efficacy of HSP90 inhibitors could be explained by various specificity of the agents towards the four HSP90 paralogs which include two cytosolic forms (HSP90α (inducible/major form) and HSP90β (constitutive/minor forms), 94-kDa glucose-regulated protein (Grp94) in the ER (endoplasmic reticulum), and Trap1 (tumor necrosis factor receptor associated protein 1) in mitochondria [103]. The gene discussed is HSP90AA1; the disease is cancer.