The GSHP dogs with this gene variant have altered expression of the C-terminal tail of the UNC93B1 protein, and protein modeling studies predict that this altered expression may allow the UNC93B1 protein to interact with TLR7, but not syndecan binding protein.10 Therefore, because the variant leads to an amino acid substitution, it is possible that the normal interaction between TLR7 and UNC93B1 is not dampened, leading to the potential for development of autoimmunity. The gene discussed is UNC93B1; the disease is Autoimmunity.