By applying gene set variation analysis to multiple publicly available datasets, they showed that all four IFN signatures, especially the IFNβ1 signature, were highly enriched in skin and synovium of SLE patients, whereas all signatures were relatively less enriched in the kidney (both the glomerulus and tubulointerstitium) of lupus nephritis (LN) patients. Here, IFNA1 is linked to lupus nephritis.