Perhaps the impact of mDia1 in this setting is RAGE independent; for example, these findings might suggest that mDia1 contribution to the neuropathy pathogenesis might be a result of its primary, rho-mediated cytoskeleton regulatory functions (Rose et al. 2005; Shinohara et al. 2012), and is complementary to RAGE-stimulated phosphorylation of Akt (protein kinase B) and cell proliferation/migration observed in other cell types such as smooth muscle cells (Rai et al. 2012). Here, AGER is linked to neuropathy.