RHO and endothelial dysfunction: A direct role of GEF-H1 in agonist-induced, Rho-dependent and MT disassembly-driven endothelial dysfunction has been clearly elucidated with the findings that knockdown of GEF-H1 attenuated thrombin- or nocodazole-induced EC barrier disruption, while overexpression of wild type GEF-H1 exacerbated such barrier disruptive effects (Birukova et al., 2006).