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. The gene discussed is ERBB2; the disease is neoplasm.