As SPOP has been characterized as a bona fide E3 ligase that governs BRD4 protein stability in prostate cancer,[29, 30, 31] and BRD4 cooperates with EWS–FLI1 to regulate the EWS–FLI1‐mediated transcriptional programs in Ewing sarcoma,[32] we examined if BRD4 is involved in SPOP‐depletion‐induced Ewing cell growth control. Here, FLI1 is linked to prostate carcinoma.