RELB and breast carcinoma: Xu et al. (2007) showed that RelB triggered by radiation resulted in the protection of irradiated cells, whereas vitamin D3 ablated this protection. As a member of the NF-κB family, RelB can be inactivated by VDR-mediated transcriptional repression. Similarly, in breast cancer cells pre-treated with vitamin D3, sensitivity to radiation was increased accompanied with down-regulation of RelB (Mineva et al., 2009), again indicating that RelB was a target gene regulated by vitamin D in response to radiation.