Update publication information. As the most life-threatening subtype of pediatric medulloblastoma (MB), MYC-amplified Group 3 (G3) MB lacks effective and selective therapeutics. We tried to indirectly target MYC (oncogenic driver and cancer-dependent molecule) production via inhibiting translational machinery. Through multiple datasets analyses on components of eIF4F (eukaryotic translation initiation factor 4F) complex, we found that EIF4A1 (major component with RNA helicase activity) has relatively higher expression level and the closest positive correlation with MYC in G3-MB among normal control and other 3 subtypes (e.g., WNT, SHH and G4). Both in vitro and in vivo experiments with MYC-amplified G3-MB cell lines showed effective growth inhibition upon EIF4A1 knockout or inhibitor treatment. Further FACS analysis found decreased cell proliferation and enhanced apoptosis on EIF4A1 inhibitor treatment. To explore the mechanisms of EIF4A1 inhibition on arresting MYC-amplified G3-MB, we performed the whole proteome analyses on corresponding MB cells treated with EIF4A1 inhibitor.