In vivo, two studies evaluated the anti-tumour activity of either ipatasertib or capivasertib (both ATP-competitive AKT inhibitors) found that although these drugs showed growth suppression in a range of human xenograft models with AKT-activating lesions, regressions were more commonly observed in tumours with homozygous PTEN inactivation compared with those with activating PIK3CA mutations [29,30]. The gene discussed is AKT1; the disease is neoplasm.