AR and cancer: THZ1, on the other hand, inhibits CDK7-mediated phosphorylation of MED1 at threonine 1457, a modification critical for MED1’s functional role in enhancing AR-driven transcription in PCa cells.599 By suppressing MED1 hyperphosphorylation, THZ1 disrupts the interaction between MED1 and AR, resulting in a significant decrease in the expression of AR target genes.600 This disruption leads to diminished formation of MED1 condensates, reduced transcriptional activation, and impaired proliferation of cancer cells.601