To investigate the underlying molecular mechanism(s) responsible for differentiation-dependent type I IFN responsiveness in human neuronal cells, we utilized a previously established culture system based on the neuroblastoma cell line BE(2)-C [6] and focused on canonical type I IFN signaling pathway components, including the surface receptor heterodimer composed of IFNAR1 and IFNAR2, the receptor-associated signal transduction kinases Jak1 and Tyk2, and the transcription factors IRF-9, STAT1, and STAT2. The gene discussed is STAT2; the disease is neuroblastoma.