Given the central role of BCMA and its ligands BAFF and APRIL in the dysregulated B cell homeostasis observed in SLE, we investigated the complex interplay between BCMA expression on peripheral blood B cells subsets, soluble BCMA plasma concentrations and clinical disease variables as well as peripheral blood plasmablast expansion, a hallmark of the disease. This evidence concerns the gene TNFRSF17 and systemic lupus erythematosus.