Preclinical and clinical evidence showed that the co-inhibition of the AR axis and PARP generates a combined anti-tumor effect: PARP is involved in the positive co-regulation of AR signaling, and thus, PARP/AR signaling co-inhibition leads to enhanced AR target gene suppression; moreover, treatment with NHAs inhibits the transcription of some DDR genes, inducing synthetic lethality due to cancer cells’ inability to repair DNA, even in patients without any DDR alterations [86]. Here, AR is linked to cancer.