HDAC6 and glioblastoma: Because the enzyme activity of CNOT6 is required for deadenylation by the CCR4-NOT nuclease complex [36], and acetylation enhances CNOT6 activity inducing RNA degradation [22], we predict that high levels of HDAC6 in GBM cells inhibit CNOT6 acetylation, leading to LINC00461 stabilization, while MPT0B291 treatment induces CNOT6 acetylation, promoting LINC00461 degradation (Fig. S7B).