Subcutaneous administration of CSL362 in cynomolgus macaques depleted plasmacytoid dendritic cells and basophils and inhibited TLR9-induced IFN-inducible gene expression, strongly suggesting that CSL362 antibody and more widely basophil and pDC depletion may represent an interesting therapeutic option for SLE patients that requires further investigation (Figure 1) [77]. The gene discussed is TLR9; the disease is systemic lupus erythematosus.