Together, our results provide novel pharmacological strategies against Ras-pathway activated cancers and a mechanism for cross-activation between the Ras/Raf/MEK/ERK and PI3K/AKT/mTOR pathways via a Ras˧PIK3IP1˧PI3K signaling network, which promises further insight into the role of this signaling network in regulating cross-talk known to drive response and resistance to clinically relevant targeted therapies. The gene discussed is AKT1; the disease is cancer.