Disrupting such IP3R/Bcl-xL complexes could therefore result in Ca2+-driven cell death, as observed in several Bcl-2-dependent cancer in which Bcl-2 was displaced from IP3Rs [22, 58] or antagonize breast cancer cell migration, a process controlled by Bcl-xL at the level of the IP3R [42]. This evidence concerns the gene BCL2 and breast cancer.