The IFN-I signature may be driven in part through engulfment of dead cells by macrophages and dendritic cells.33 The increased rate of cell death of neutrophils in patients with SLE, as well as the increased cell death of CD4–CD8– TCR-αβ+ T cells in MRL-lpr mice and human SLE T cells, may both contribute to the source of dead cells. The gene discussed is CD4; the disease is systemic lupus erythematosus.