The observed signalling impairments were associated with impaired in vitro insulin-stimulated glycolysis, fasting hyperinsulinemia and reduced insulin-stimulated skeletal muscle glucose uptake in vivo, and thus are likely to contribute to the insulin resistant phenotype of the carriers of p.P50T/AKT2 variant (Latva-Rasku et al. 2018). Here, AKT2 is linked to hyperinsulinism.