These findings suggest that BCL2A1 suppresses intrinsic cell apoptosis under stress conditions by interacting with the BH3-only protein of activator BID to inactivate BAK/BAX in mitochondrial outer membrane permeabilization (MOMP) [33] and two pro-apoptotic proteins, HRK/BAD [34], in the mitochondria of ovarian cancer cells. This evidence concerns the gene BAK1 and ovarian carcinoma.