CTLs share a wide range of molecular signatures that allow these cells to directly mediate the killing of tumor cells after the recognition of target cells, such as the granule cytosolic pathway (e.g., perforin/granzyme) and the death receptor pathway [e.g., FAS/Fas and Fas ligand (FasL), TNF-related apoptosis-inducing ligand (TRAIL)/TRAIL receptor (TRAIL-R)] [2, 4]. The gene discussed is FAS; the disease is neoplasm.