Thus, tumor suppressors and proapoptotic molecules like BRCA1 or PTEN bind to IP3R to boost Ca2+ ion uptake at MAMs while tumor promoters and anti-apoptotic molecules such as Bcl2 or Bcl-xL repress mitochondrial Ca2+ ion overload by binding to and inhibiting the channel activity [438,439]. Here, ITPR1 is linked to neoplasm.