Tumor cell upregulation of anti-apoptotic factors such as Bcl-2 has been demonstrated to be higher in bone metastases compared to other soft tissue metastases in prostate cancer patients [175] and given it has been suggested that inhibition of Bcl-2 can sensitize tumor cells to T-cell mediated killing [176], upregulation of Bcl-2 family proteins may be another mechanism by which tumors can overcome immune-mediated dormancy and suppression of growth in the bone. This evidence concerns the gene BCL2 and prostate carcinoma.