AKT1 and neoplasm: Pathways that were previously thought to be universally targetable have proven to be difficult to treat, such as the phosphatidylinositol 3-kinase/AKT pathway,29 or subject to variation in results by tumor type, such as BRAF30 or HER2/3 mutations.31,32 In protocol patients, we were unable to ascertain any strong individual signals of activity for particular alterations in specific tumor types in part because of insufficient numbers of patients.