A correlation of the resultsof Tables 1, 2, and 6 indicates that theadducts (1, 2, 4–6, 9, and 10) aswell as tazemetostat solely acting as EZH2 inhibitors were unableto exert cell growth inhibitory effects and modulation of both thetargets (EZH2 and HSP90) was mandatory for the anti-GBM efficacy.Notably, compounds 3, 7 and 8 which can be categorized as dual inhibitors were the only ones toexert cell viability inhibitory potential. This evidence concerns the gene HSP90AA1 and glioblastoma.