RRAD (Ras associated with diabetes) is a small GTP-binding member of the RAS superfaily that was originally as being overexpressed in skeletal muscle of people with type II diabetes (Reynet and Kahn, 1993; Zhu et al, 1995). RRAD has roles in cardiac regulation, and contributes to glucose metabolism and tumor metastasis through interaction with NME1 (nucleoside diphosphate kinase A) (Chang et al, 2007; Wang et al, 2010; Zhu et al, 1999; Tseng et al, 2001). In addition, RRAD contributes to Schwann cell development and myelination by modulating the RHO ROCK pathway (Ward et al, 2002; Yamauchi et al, 2004; Melendez-Vasquez et al, 2004). RRAD gene expression is positively regulated upon binding of EGR1 or EGR2 to their cognate sites in the promoter, while EGR-dependent recruitment of NAB proteins leads to EGR-mediated repression through the recruitment of chromatin remodellers and histone deacetylase complexes (Svaren et al, 2000; Mager et al, 2008). RRAD expression is repressed in Schwann cells during myelination and is upregulated in NAB knockout mice, implicating NAB proteins as negative regulators of RRAD expression (Verheijen et al, 2003; Mager et al, 2008; Desmazières et al, 2008). It is worth noting, however, that a number of genes required for Schwann cell differentiation and myelination are activated by EGR:NAB complexes at their promoters (Le et al, 2005).