Despite this finding of efficient nuclear proteasomal degradation of AR in prostate cancer models, the observation that the inefficient proteasomal degradation of polyQ-AR contributes to its aggregation (Heine et al., 2015), and that enhancing nuclear export of polyQ-AR substantially enhances its proteasomal degradation (Arnold et al., 2019), suggests that polyQ-expanded AR is more efficiently degraded by proteasomes within the cytoplasmic compartment. The gene discussed is AR; the disease is prostate cancer.