Mechanism of induction and inhibition of pro- and anti-apoptotic proteins by p53 and induction of apoptosis. Taken and modified from Aubrey et al. [20] and Giam et al. [21]. Activation and inhibition of pro-apoptotic and anti-apoptotic proteins, respectively, through the conformational change of Bax, facilitating the permeabilization of the mitochondrial membrane by pore formation, and, consequently, the release of cytochrome c from the mitochondria to the cytosol forming the apoptosome together with cytosolic Apaf-1 and pro-caspase-9, triggering regulated death. Appreciation of the morphological and biochemical changes of apoptosis. Bad: Bcl-2 agonist of cell death; Bak: Bcl-2 antagonist killer 1; Bax: Bcl-2-associated X protein; Bcl-xL: B-cell lymphoma-extra-large; Bcl-2: B-cell lymphoma 2; Bim: Bcl-2 interacting mediator of cell death; Caspase -3, -6, -7, -9: Cysteinyl aspartic acid-protease -3, -6, -7, -9; Mcl-1: Myeloid cell leukemia-1; PUMA: p53 upregulated modulator of apoptosis.