were 40 and 60-fold less, respectively, than in the parent HiBiT-BRD4 cells (Dmax 50 = 23 vs 0.6 nM, and 38 vs 0.6 nM, respectively, Figure ). This implies that 27 is almost equally reliant on VHL and CRBN to drive the degradation of BRD4, but performing slightly worse in CRBN KO cells than VHL KO or parental cells, and so showing a slight preferential reliance on CRBN. The rate of degradation (λ) for both VHL and CRBN KO cells lines is 2-fold slower than in parental cells (λmax = 1.2 and 1.0 h -1 , vs 2.3 h -1 , Figure ). Remarkably, the sum of the rate constants from 27 in both VHL and CRBN KO cells equal the rate constant in the parental cells, indicating that both VHL and CRBN are contributing to the degradation of BRD4 in an additive fashion.