Similarities to muscle disease exist in the skin: first, vasculopathy and vascular deposition of complement components can be detected in cutaneous DM skin [13], [14]; second, there is damage to the parenchymal cells (e.g. keratinocytes) [11]; third, DM skin appears to be characterized by increased abundance of several gene products that are known to be upregulated by IFN [15], [16] as well as by increased numbers of plasmacytoid dendritic cells [17], [18]. Here, IFNA1 is linked to dermatomyositis.