In prostate cancer cells, ARv7 stems from aberrant messenger RNA splicing of AR exons 1 to 3, loss of exons 4 to 8, and inclusion of cryptic exon 3 into the transcribed AR gene.24,25 Consequently, the affected protein is constitutively active in the absence of androgens and facilitates the growth of prostate cancer in the presence of antiandrogens.26,27 We found AR expression in 40% of metastatic LCT without the ARv7 splice variant, which indicates a potential for treatment with antiandrogens. This evidence concerns the gene AR and Familial prostate cancer.