To provide further evidence that SKIP is a co-activator of AR function, the effects of SKIP overexpression on AR–dependent transcription were assessed using the androgen-responsive mouse mammary tumour virus (MMTV) MMTV-luc and the prostate-specific antigen (PSA) PSA-luc luciferase reporter plasmids in a prostate cancer cell line. This evidence concerns the gene KLK3 and prostate carcinoma.