Anti-cancer treatments may also generate extrinsic apoptotic signals, e.g., by increasing the expression of death receptors or cytotoxic ligands, including TNF, TRAIL, or Fas ligand (FasL); if released by infiltrating immune cells or the cancer cells themselves, this may activate death receptor signaling in an auto- or para-crine manner [2,12,53]. This evidence concerns the gene FASLG and cancer.