SOAT1 and cystic fibrosis: To assess whether STAT phosphorylation was dependent on the activation of JAK/STAT signaling pathway by IFN-β through activation of IFN-β receptor (IFNAR), CF were pretreated with 100 or 500 nM of JAK inhibitor Ruxolitinib, which inhibited IFN-β-induced STAT1, STAT2, and STAT3 protein phosphorylation (Figures 1D–F).