Altogether, we were able to demonstrate that poly(A) tail length modulation can be achieved using chemical inhibitors. Indeed, our inhibitors confirm that NOT9 plays a role in the deadenylation of specific mRNAs either through binding to them in a non-specific fashion for general bulk deadenylation or by recruitment of RNAbinding proteins for which the inhibitory peptides do not discriminate. Future work will aim at developing ligands for other binding sites on the CCR4-NOT complex to further dissect their roles and therapeutic value. We envision that different sites will have effects on different mRNA subsets and that treating cells with different inhibitors will be able to highlight their individual roles in healthy physiology as well as pathogenesis and thereby provide novel therapeutic strategies.