We previously showed that activated AR can directly target miR-1 and that miR-1 functions as an inhibitor of prostate cancer bone metastasis.20 Accordingly, we analyzed the relationships between the genes associated with high miR-1 expression and androgen-responsive gene signatures27 in the Taylor Prostate Cancer Dataset.28 By using a bioinformatics approach, GSEA, we determined an association between KLF4 expression and AR-induced miR-1 expression (Supplementary Figures S3A,B). This evidence concerns the gene AR and prostate cancer.