Human diseases are often driven by abnormal gene regulation.  This involves DNA binding transcription factors (TFs) that begin misinterpreting the genetic information.  The Androgen Receptor (AR) is one such TF responsive to testosterone in male-specific organs, and the AR goes rogue in the context of prostate cancer.  The Gryder lab has discovered new mechanisms by which the AR rewires the genome and the 3D epigenome in prostate cancer.  We have developed a new chemical probe that causes the AR to shutdown 3D loops between enhancers (long-range regulatory DNA elements) and target genes. Furthermore, we are exploring the role of liquid-liquid phase separation as a mechanism for the formation of 3D clusters in the prostate cancer epigenome, providing new clues as to how molecular assembly at key genetic locations is occurring, and how drugs may act upon these clusters for therapeutic benefit.