Through research with SLC15A4-mutant or SLC15A4-deficient mice, lack of SLC15A4 has been linked to impaired nucleotide oligomerization domain-1 (NOD1)-, toll-like receptor 7 (TLR7)-, and TLR9-dependent cytokines such as type 1 interferon (IFN), all of which are indispensable to the pathogenesis of SLE (Sasawatari et al., 2011; Baccala et al., 2013; Kobayashi et al., 2014). This evidence concerns the gene SLC15A4 and systemic lupus erythematosus.