Second, because the observed phenotype is routed in aberrant myeloid cell function, which secondarily stimulates B- and plasma-cell autoimmunity, and because macrophages of young MCPIP1-deficient mice displayed inducible overexpression of TLR-7 (Fig. 1), we speculated that macrophages would upregulate B-cell-activating factors upon stimulation with TLR-7 (R848) and TLR-9 (CpG) ligands. The gene discussed is TLR7; the disease is Autoimmunity.