This discrepancy is likely due to a number of different factors including the poor predictive value of some pre-clinical models, the complexity of the PI3K pathway and the impact that co-occurring mutations of several pathway components may have on response to inhibition of a single node, as well as the differences in the pharmacological requirements that define the anti-tumour activity of individual AKT inhibitors. The gene discussed is PIK3CA; the disease is neoplasm.