High vitamin D exposure is hypothesized to decrease cancer risk, possibly through genomic effects modulated by the vitamin D receptor, and by autocrine/paracrine metabolism of the vitamin D receptor’s ligand, 1α,25-(OH)2-vitamin D3.49 Recently, an increasing number of studies have examined polymorphisms in vitamin D receptor and selected genes in the vitamin D pathway in relation to colorectal, breast, and prostate cancer risk.48 However, there is currently no strong, consistent epidemiologic evidence for a substantial influence of any single variant in vitamin D pathway genes on cancer risk. This evidence concerns the gene VDR and prostate carcinoma.