While prostatic cancer is usually thought of as an androgen dependent disease, it has recently become clear that numerous other hormones including 1 alpha,25-dihydroxyvitamin D3 (1,25D) can regulate its growth and differentiation. This commentary reviews the epidemiological evidence supporting a role for 1,25D deficiency in the genesis of prostatic cancer, the effects that this hormone has on benign and malignant prostatic epithelial cells in culture, the mechanisms through which it produces these effects and the potential clinical utility of 1,25D and its non-hypercalcemic analogs in the prevention and treatment of this increasingly common disease. While a wide body of information exists regarding the actions of vitamin D in other organ sites, this review addresses only prostatic studies. The substantial nature of the current information suggests that we have arrived at a point where we can no longer think of prostate cancer solely in terms of its response to androgens.