In line with this observation, the presence of SNPs and rare variants in genes involved in type I IFN signaling and antiviral pathways, namely IRF-8, STAT3, SOCS1, TYK2, ZC3HAV1, and OAS1, which may display transcriptional dysregulation in blood cells at distinct MS stages (10), were found to be altered by several published GWA studies in MS, confirming the hypothesis that an alteration of IFN-regulated antiviral responses could be linked to MS pathogenesis (11–13). This evidence concerns the gene STAT3 and myeloid sarcoma.