UNC93B1 and systemic lupus erythematosus: For example, a TLR7 gain-of-function genetic variation (34) and overactive TLR7 pathway as a result of variants in UNC93B1, which binds TLR7 and is essential for TLR7 trafficking to the endosome (35, 36), have provided direct evidence that genetic variants related to TLR7 activation trigger human SLE pathogenesis.