On the basis of previous studies showing that AR binding to its target genes through the DBD is critical to SBMA pathogenesis (17) and that disrupting the interaction between AR and its transcriptional coregulators represents a promising therapeutic strategy for this disease (17, 22, 23, 33), we reasoned that overexpression of AR45 would be able to counteract SBMA toxicity. Here, AR is linked to Kennedy disease.