On the other hand, the induction of Gal-9 transcription by HCMV and UV-HCMV which is known to be dependent on both IRF3-mediated type I IFN production and JAK/STAT signaling in this system [39], was elevated post infection in the primary HFs but not in either of the IFN-abrogated cell lines (Figure 1). The gene discussed is IFNA1; the disease is infection.