Interaction between GRK2 and Akt has been shown to suppress Akt kinase activity, contributing to endothelial dysfunction in diabetes and metabolic disorders (Taguchi et al., 2011; Taguchi et al., 2012a; Taguchi et al., 2012b; Taguchi et al., 2015; Taguchi et al., 2017; Gurevich et al., 2016; Bencivenga et al., 2021). This evidence concerns the gene AKT1 and metabolic disease.