Similarly to 17AAG, numerous other HSP90 inhibitors were able to suppress GBM growth and progression either in vitro, by inhibiting several key oncogenes and regulators of GBM biology, which are direct HSP90 client proteins, or in vivo, by inducing tumor regression in GBM-bearing mice and increasing animal survival [42,43,44,45]. The gene discussed is HSP90AB1; the disease is neoplasm.