Given the importance of 4E-BP1-regulated cap-dependent translation as a common downstream node that integrates multiple oncogenic signaling pathways for tumor growth and metastasis [11, 19, 44], compounds that mimic 4E-BP1 biochemical function by disruption of eIF4E-eIF4G interaction or target other translation initiation components may be effective for cancer therapeutics. Here, EIF4G1 is linked to neoplasm.