Par-4 overexpression has been shown by Boehrer et al. to augment the apoptotic death of Jurkat T cells induced by TNF related Apoptosis Inducing Ligand (TRAIL). Previously, the same authors have demonstrated a parallel augmentation of chemotherapeutic drug-induced apoptosis in the same cell line overexpressing Par-4. Through these and other studies, Par-4 appears to emerge as a general intracellular facilitator of both extrinsic and intrinsic pathways of apoptosis. The ability of Par-4 to modulate relevant inhibitors of apoptosis and to facilitate activation of alternative initiator or executioner caspases in contingent situations may support its role as a common facilitator/enhancer of apoptotic cell death. Further understanding of Par-4 biology will have significant clinical implications especially in overcoming drug resistance phenomenon in cancer.