In this regard, the capacitative Ca2+ entry that has been shown to block the development of the apoptosis resistance phenotype such as that seen in Bcl-2 over-expressing LNCaP cells [54,55] may be equivalent to the elevated homeostatic Ca2+ level induced by T and 1,25(OH)2D3, suggesting that adequate levels of the two hormones should also prevent the development of the apoptosis-resistant, or castration resistant, phenotype in prostate cancer. Here, BCL2 is linked to prostate cancer.