In tumorigenesis, apoptosis is suppressed in an orchestrated manner through upregulations of anti-apoptotic proteins B-cell lymphoma 2 (Bcl-2), B-cell lymphoma-extra large (Bcl-xL), B-cell lymphoma-w (Bcl-W), and induced myeloid leukaemia cell differentiation protein (Mcl-1), and the downregulation of pro-apoptotic proteins Bcl-2 associated X protein (Bax), Bcl-2 interacting protein (Bim), Bcl-2 homologous antagonist/killer (Bak), BH3-interacting domain death agonist (Bid), and NOXA in the intrinsic mitochondrial apoptotic pathway to promote sustained tumor growth [42,43,44,45,46]. Here, BAK1 is linked to neoplasm.