Harmol can induce autophagy and suppression of survivin expression, subsequently induce apoptotic cell death in U251MG human glioma cells [12] and apoptosis by caspase-8 activation independently from Fas/Fas ligand interaction in human non-small cell lung cancer (NSCLC) H596 cells [13], and significantly inhibit the dioxin-mediated induction of CYP1A1 at mRNA, protein, and activity levels in a concentration-dependent manner in human and murine hepatoma cells [14]. The gene discussed is FAS; the disease is central nervous system cancer.