Innate or adaptive immune cells are primarily activated and respond to infection by generating a milieu of cytokines—principal among which are IFNs (type-1/type-II).37,38 Analogously, SLE and LN are well-understood states of IFN excess,39, –41 and stigmata of IFN excess—tubuloreticular inclusions in glomerular endothelial cells—are typically associated with APOL1-FSGS. The gene discussed is APOL1; the disease is focal segmental glomerulosclerosis.