Indeed, pathologically, Bcl-2 overexpression is typically observed in tumor-wide and it is well known to be a cause of treatment-resistant, meanwhile, Bcl-2 suppression by VD3 has been reported in multiple tumor types including prostate cancer [32, 37–39], suggesting that the relationship between VD3 and Bcl-2 could be common in tumor-wide. Here, BCL2 is linked to neoplasm.