In our effort to augment the efficacy of GSCs treatment through MAGL targeting, as elucidated in our previous research, and to circumvent potential translational obstacles arising from the nonspecific effects of MAGL inhibitors, we proposed to enhance the specificity of MAGL targeting intervention by incorporating the ligand of the highly expressed MDM2 E3 ligase in GBM into the design of the PROTAC. The gene discussed is MDM2; the disease is glioblastoma.