However, genetic manipulation of Arg-I (partial deletion) in Arg-II deficient mice shows that upregulation of vascular Arg-I, rather than Arg-II, contributes to the diabetes (type I)-induced endothelial dysfunction, vascular stiffness, and coronary fibrosis (146), in which Rho kinase activation can be responsible for the observed pathophysiology (147). Here, LNCARGI is linked to diabetes mellitus.