More importantly, GRK2 inhibition or partial GRK2 deletion improved the endothelial dysfunction observed in obese/diabetic (Taguchi et al., 2011b, 2012c, 2013) or hypertensive (Avendano et al., 2014) animal models by restoring the impaired Akt/eNOS pathway and NO availability in a process in which glucose homeostasis may be implicated (Taguchi et al., 2017). The gene discussed is GRK2; the disease is endothelial dysfunction.