The GWAS correlation of TNIP1 sequence variants to several autoimmune diseases [17–19, 22, 26], for example, and evidence of NF-κB signaling possibly under TNIP1 control post-TLR signaling [10, 19, 26, 50, 95] provided rationale for investigating SLE-like characteristics in knockout or mutant knock-in mouse models, respectively, with missing or dysfunctional TNIP1 protein. The gene discussed is TNIP1; the disease is autoimmune disease.