treating cells with HDAC6 inhibitors, MP0B291 and trichostatin A, led to a decrease in the interaction of HDAC6 and CNOT6 in cells (Fig. S3A), suggesting that deacetylase activity is essential for HDAC6 to bind CNOT6, causing changes in the deadenylase activation.we predict that high levels of HDAC6 in GBM cells inhibit CNOT6 acetylation.Although our current results prove that HDAC6 inhibition increases CNOT6 and decreases FUS protein levels, further studies are needed to confirm whether HDAC6 directly regulates the lysine status of these two proteins.