the CRBN ligand with a DCAF11 recruiter shifted selectivity from HDAC6-specific to pan-HDAC degradation. This change in the selectivity profile creates new opportunities to investigate and compare HDAC isoform-specific or general effects. Importantly, PROTACs affect not only the enzymatic but also the non-enzymatic functions of their targets. While HDAC6 selective degraders allow for a more detailed assessment of HDAC6 function in pathology and physiology, a pan-HDAC degrader may provide a more general picture of HDACs functions across isoforms and may also reveal isoform synergies in terms of phenotypic effects such as anticancer activity. In addition, both approaches may have potential clinical applications. While pan-HDAC degraders could be developed to treat multiple cancers , selective HDAC6 PROTACs, like selective HDAC6 inhibitors , could be used in neurodegenerative diseases, inflammatory diseases, and some cancers. In the latter case, it would be important to replace the non-selective HDAC inhibitor warhead in A6 with a selective HDAC6 inhibitor scaffold to avoid class I effects resulting from HDAC inhibition.