The potential mechanisms of caspase-3 in relation to poor DFS in BMSCC patient with postoperative RT could be that activated caspase-3 cleaves cytosolic calcium-independent phospholipase A2 (iPLA2) in dying tumor cells or tumor stromal cells in response to radiation [28, 39] to generate arachidonic acid, which is the precursor for the synthesis of prostaglandin E2 (PGE2) mediated by cyclooxygenase-1/-2 (COX1/2) [40]. The gene discussed is CASP3; the disease is neoplasm.