Preclinical data have demonstrated that inhibition of AKT activity, through mTORC2 inhibition, may block tumour progression.13 Subsequently, a new generation of mTORC1/2 inhibitors have been developed, as dual inhibition may offer an advantage over mTORC1 inhibitors by targeting at least three key enzymes (PI3K, AKT and mTOR).14 Proof of this concept was demonstrated in preclinical models for several epithelial malignancies.15–18. The gene discussed is AKT1; the disease is neoplasm.