The transcription factor Etv3 is a key regulator of the tolerogenic function of dendritic cells (DCs), which help maintain immune tolerance in a normal state.[1] Etv3 is predominantly expressed in mature DCs, especially migratory DCs (migDCs), and its expression increases during DC maturation in both mice and humans.[1] Mice with global or DC-specific deletion of Etv3 show expansion of low-CD25 regulatory T cells, spontaneous activation of conventional T cells, and T cell infiltration into multiple organs.[1] Etv3 ensures optimal homing of migDCs, promotes their CCR7-dependent migration, and maintains regulatory T cells, thereby preventing systemic autoimmunity.[1] A single base polymorphism (SNP) in the 5′ unregulated region of human ETV3 is associated with systemic lupus erythematosus (SLE) and results in reduced levels of ETV3 transcripts in human DC cultures.[1] Loss of Etv3 exacerbates SLE-like disease and explains the genetic association of ETV3 with SLE.[1]