The altered composition of CRAC channels in prostate cancer with a shift in Orai1:Orai3 ratio and distinct pharmacological profiles open the possibility to selectively manipulate ICRAC activity in cancer cells (e.g. to higher Ca2+ signals and thereby drive cancer cells into apoptosis) without effecting Ca2+ signals in non-cancerous cells. This evidence concerns the gene ORAI1 and Familial prostate cancer.