Research has indicated that celastrol, combined with 17-N-Allylamino-17-demethoxygeldanamycin (17-AAG), inhibits the toxic stress response of HSP90-targeted proteins, reduces the sensitization of human glioblastomas to celastrol treatment, and increases the accumulation of polyubiquitylated aggregates and p62, thereby enhancing protein stability and overcoming multidrug resistance (MDR) in glioblastoma 128. The gene discussed is SQSTM1; the disease is glioblastoma.