c-Rel-deficiency leads to altered phenotypes in many disease models: c-Rel KO mice are resistant to EAE, an autoimmune model of multiple sclerosis driven by Th17 cells (Chen et al., 2011); c-Rel KO mice fail to develop severe colitis induced by treatment with dextran sodium sulfate (DSS)(Luu et al., 2017), perhaps also as a result of loss of Th17 cell development (Chen et al., 2011); and overexpression of c-Rel has been shown to protect human islets from cell death mediated by the cell death protein PDCD4 via an increase in microRNA-21 expression (Ruan et al., 2011b). The gene discussed is REL; the disease is multiple sclerosis.