The development of these inhibitors, as well as neddylation inhibitors, stems from the observation that overexpression of cullins has been reported in several types of cancer.52 We have previously observed that the inhibition of neddylation promoted spastin stability.19 As positive regulation by neddylation is a general pathway shared by several cullins, we searched for a more specific cullin-mediated pathway that controls spastin stability and demonstrated an important role played by CRL4. Here, CACUL1 is linked to cancer.