In a tumor context, the overexpression of XBP1 in breast cancer cells increased levels of Bcl-2, inhibiting apoptosis, but JNK can phosphorylate and inhibit Bcl-2, showing how the effects of IRE1 can vary depending on the output: pro-apoptotic when mediated by JNK and anti-apoptotic when mediated by XBP1 splicing. This evidence concerns the gene BCL2 and neoplasm.