FASLG and neoplasm: This approach takes advantage of their antitumor effector functions via distinct mechanisms, including (a) granule exocytosis resulting in the release of perforin and granule-associated enzymes (granzymes) and (b) release of exosomes containing Fas ligand (FasL) and tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), leading to the predominantly programmed apoptotic tumor cell death process (1).