Ligand binding leads to dimerisation of the type I IFN receptor subunits IFNAR1 and IFNAR2 and causes their conformational change. The JAK kinase Tyk2, which is constitutively bound to IFNAR1, phosphorylates the receptor at tyrosine residues and creates a docking site for STAT2. Subsequently, Tyk2 phosphor-ylates STAT2 at Y690. At the same time the receptor-bound JAK1 phosphorylates STAT1 at Y701 [15, 16] .