IFN beta elicits a markedly higher antiproliferation response in some cell types such as, embryonal carcinoma, melanoma and melanocytes than do IFN alphas. Higher potency of IFN beta in treatment of multiple sclerosis and certain cancers has been observed. Type I IFNs signal through binding to a common cell surface receptor. Two chains of the receptor, IFNAR1 and IFNAR2, have been identified. Both chains are necessary for function and in the absence of either there is neither high affinity binding nor biological activity. The intracellular portions of the receptor subunits are bound by tyrosine kinases, Jak1 and Tyk2, members of the Janus kinase family. Upon ligand binding these kinases are activated and phosphorylate members of the STAT family of transcription factors, as well as IFNAR1 and 2.