Different from temporary IFN-α induction by viral nucleic acids during viral infection, the exposure to endogenous nucleic acids from dead cells in SLE results in sustained IFN-α production mainly by plasmacytoid dendritic cells (pDC) and neutrophils, and the presence of a broad IFN-inducible genes (IFIG) expression signature in these cells [34, 37]. The gene discussed is IFNA1; the disease is viral infectious disease.