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On the basis of the evidence available, we hypothesise that direct stimulation of the more proximal L-cells is the predominant mechanism

Notably, the identification of thalidomide and its analogs as CRBN ligands vastly expanded the E3 ligase toolbox [48], spurring a wave of VHL- and CRBN-based PROTACs such as ARV-825 and DBET1 that achieved potent degradation of BRD4 and AR in cellular models [49, 50]

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