A measurable effect of properdin deficiency on B cell expression or activity of CD21 would strengthen the rationale for targeting properdin—or indeed of the ligand C3d [31,35]—in the treatment of lupus (while C5aR blockade has been shown to alleviate blood–brain barrier leakage in lupus prone mice [36]). The gene discussed is CFP; the disease is systemic lupus erythematosus.