In an ATP-bound state, HSP90α (referred to as HSP90 in this study) adopts a closed conformation and forms a mature complex with co-chaperones to indirectly promote tumor progression by protecting and stabilizing its client proteins, such as mutated p53, HER-2, EGFR, BRAF, AKT, MET, VEGFR, FLT3, androgen/estrogen receptors, HIF-1αn and hTERT [9]. The gene discussed is HSP90AA1; the disease is neoplasm.