Three or four BH domains are possessed by most of the anti apoptotic family members, and most of them also possess a C terminal transmembrane domain that’s accountable for their localization to the cytoplasmic faces of intracellular membranes. The pro apoptotic Bcl 2 members facilitate or immediately induce the permeabilization of the mitochondrial membrane, that leads to the release of caspase activators in the mitochondria thus causing apoptosis. The pro apoptotic Bcl 2 proteins are antagonized by their anti apoptotic competitors which function by binding and sequestering the pro apoptotic Bcl 2 proteins, thus stopping mitochondrial conjugating enzyme membrane permeabilization induced apoptosis. In mouse and human, there are 6 known members of the Bcl2 like anti apoptotic subscription family, which are imperative to the growth and success of lymphoid and myeloid cells. So far, orthologues of Bcl 2, Bcl XL,Mcl 1, and NRH have been determined in fish, and duplications of some members have also occurred possibly as due to teleost specific genome duplication. NR 13 was discovered in quail neuroretina cells as a gene that was induced by Rous sarcoma virus infection. NR 13 gene activation by P60v src or vrel continues to be documented and accounts for the apoptotic inhibition Mitochondrion associated with viral pathogenesis or oncogenesis, respectively. Subsequent reports of NR 13 orthologues in animals proved their jobs as antagonists of apoptosis. Recently, the zebrafish NR 13 orthologue was identified, which was shown to play a key role in development, and antagonize the professional apoptotic Bax. Zebrafish orthologues of Mcl 1 and Bcl XL are also recognized. Along with the anti apoptotic features of Mcl 1 and Bcl XL noticed in zebrafish embryo, over expression of both zebrafish Mcl 1 or Bcl XL secured betanodavirusinfected GL av cells from necrotic cell death. Several pathogen associated molecular patterns, including lipopolysaccharide and double-stranded RNA, are identified inducers of apoptosis using types of fish cells. For instance, in fish lymphocytes, LPS induced apoptosis was found to be connected with down regulation of anti apoptotic Bcl up and 2 expression regulation in proapoptotic Bax expression. The apoptotic effect of polyriboinosinic polyribocytidylic acid has also been demonstrated using rainbow trout macrophage RTS11 cells. In several in vivo studies, similar PAMPs have been used to generate ubiquitin ligase activity immune responses in the host. Our past useful genomic reports involving Atlantic cod stimulated with immunogens led to the identification of numerous expressed sequence tags which can be mixed up in Atlantic cod implicit resistant tissue response. As the analysis of functional annotations associated with major BLAST visits of these previously produced Atlantic cod ESTs suggested the involvement of apoptotic regulation in cod immune reaction to bacterial and viral stimuli, further studies are required to completely understand the part of apoptotic regulation in cod innate immunity.