Benign prostatic hyperplasia and prostate cancer are fueled by androgens that also facilitate the expression of TMPRSS2. Previous studies have reported an inverse relationship between the number of CAG repeats in the androgen-receptor gene and the level of androgen-receptor transcriptional activity; a shorter CAG repeat length in the first exon of the androgen-receptor gene is associated with androgen hypersensitivity. The gene discussed is AR; the disease is prostate carcinoma.