Similarly, uprosertib treatment has been shown to cause dose-dependent hyperglycaemia and reduced glucose uptake in patients with gynaecological malignancies.22,23 Glucose carbon entry into the TCA cycle via PDH was also inhibited by uprosertib, consistent with previous work that suggests a direct interaction between PDH subunit B and AKT1 and that silencing of AKT1 could reduce PDH flux from 13C labelled glucose.35 By contrast exogenous lactate incorporation into citrate was maintained in cells treated with uprosertib. This evidence concerns the gene PDP1 and Hyperglycemia.