A paper by Kentsis et al. [117] has shown data demonstrating binding of ribavirin to eIF4E in multiple assays, inhibition by ribavirin of eIF4E-dependent functions in vivo, as well being able to slow tumor growth in a xenograft mouse model, suggesting that ribavirin can act like a therapeutically viable cap-analog, although this explanation for its pharmacological action has been somewhat controversial [120, 121]. Here, EIF4E is linked to neoplasm.