These prostate cancer cellular functions can be altered by the ability of ligand-activated VDR to change the expression and/or functions of many downstream key genes, for example, decrease of c-Myc [69, 70], telomerase [71], BCL-2 [72], α6 and β4 integrins [73], cyclin-dependent kinase 2 (CDK2) activity [74], and phosphorylation of the retinoblastoma protein [75], and increase of the (CDK) inhibitors p21 Waf/Cip1 and p27 Kipl [74, 76–78] and growth arrest and DNA damage-inducible gene gamma (GADD45γ) [79]. This evidence concerns the gene VDR and prostate cancer.