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During periods of mitochondrial dysfunction, toxic acyl-CoA metabolites can accumulate within the mitochondria, further inhibiting energy production and causing cellular damage

A significant portion of half sites is seen in CRPC as well, and enrichment for binding sites for transcription factors, such as HOXB13 is sustained in the cistromes for full-length AR and for ARvs in CRPC [63]

Most recently, attention has shifted to proteosomal degradation of AR, with AR-targeting PROTACs being tested as a novel therapeutic option, and with drugs that possess a dual action as AR degrader and as AR antagonist under development [24, 25]

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