Growth of prostate tumours is dependent on androgens. Hence, therapy involves removing androgens and opposing their effects using antiandrogens. This is initially successful but inevitably fails and tumours recur. The cause of this transition to hormone-independence, and the precise role of the androgen receptor in this, is a matter of considerable debate. A recent study used a mouse model to assess the effects of increased androgen receptor expression in the prostate and found that, whereas increased expression of wild-type receptor had no effect, a mutation of the androgen receptor caused it to have oncogenic properties. This goes some way to elucidating how the androgen receptor affects tumour growth, and provides an exciting model for further study of androgen receptor mutations in prostate cancer.