Model showing that disruption of calcium homeostasis leads to apoptosis by altering mitochondrial functions and inducing JNK activation. Disruption of calcium homeostasis by TG increases the intracellular free calcium level and promotes nitric oxide generation in the mitochondria and loss in mitochondrial membrane potential, leading to cytochrome c release, caspase-3 activation, induction of JNK activity, and apoptosis. Overexpression of Bcl-2 or Bcl-XL has no effect on the transient intracellular calcium levels but inhibits nitric oxide production, reduction in ΔΨm, and cytochrome c release, leading to caspase-3 activation and apoptosis.