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. This evidence concerns the gene MED1 and posterior cortical atrophy.