BCL2 and neoplasm: In response to apoptotic stimuli in many tumor cells, induced NR4A1 and NR4A3 were able to translocate from the nucleus to mitochondria, and to interact with and produce conformational changes in Bcl-2, resulting in the conversion of Bcl-2 from a protector to a killer molecule, which leading to release of cytochrome c and apoptosis of cells [19]–[21].