Previous studies in humans and mice have shown that variants in similar genes causing complete loss of trafficking proteins result in immune deficiency, whereas altered expression can cause autoimmunity.9,17 The unc-93 homolog B1 protein normally interacts with TLR7 through a syndecan-binding protein, which dampens TLR7 signaling. The gene discussed is SDCBP; the disease is Autoimmunity.