In human lupus disease, the role of pDCs is often inferred by the elevated serum level of IFN-α and upregulation of type I IFN-sensitive genes, which have been shown to correlate or associate with disease manifestations including the SLE hallmark anti-dsDNA autoantibodies, and the involvement of renal, hematological and central nervous systems [4,5,6]. Here, IFNA1 is linked to systemic lupus erythematosus.