We describe several findings related to A and B compartments, global enhancer–gene interactions, ecDNA identification at the AR locus, TAD subtypes associated with DNA alterations, transcription, epigenetic and clinical differences, as well as relationships between the 3D prostate cancer genome and SV formation, especially for the highly recurrent TMPRSS2–ERG fusion and AR amplification. This evidence concerns the gene TMPRSS2 and Familial prostate cancer.