Upon inhibition of Axl tyrosine kinase activity, R428 preferentially reduced the activation of PI3K/Akt in a dose-dependent manner, as shown in other solid tumours.34,48 Some of the downstream effects of R428 on the selected in vitro readouts of HCC tumorigenesis were evident at higher exposures (2–3 μM), which were well within the clinically achievable dose range of 1–4 μM observed in other tumour types.49 The gene discussed is AKT1; the disease is neoplasm.