While neutrophils have gained major interest as a source of interferogenic signals in SLE, including the release of genomic and oxidized mitochondrial DNA that activate plasmacytoid DCs (16–20), it is noteworthy that neutrophils are also important targets of IFN-I in this disease (16), suggesting the possibility that these cells may be an important source of autoantigens induced by IFN in SLE. Here, IFNA1 is linked to systemic lupus erythematosus.