In addition to ovarian cancer, recent studies showed that the increased expression of BRD4 was strongly associated with the initiation and progression of melanoma through promoting the expression of oncogenes, such as c‐Myc, as transcriptional regulators or epigenetic readers.[4, 6] Those findings suggest that targeted degradation of BRD4 could be a promising strategy for melanoma treatment.[40] To this end, we investigated the anti‐tumor efficacy of ARV@PDSA in B16F10 melanoma‐bearing C57BL/6 mice. This evidence concerns the gene MYC and neoplasm.