已显示eIF4E / eIF4G相互作用抑制剂4EGI-1可通过FLIP | S / L |的下调和DR5的诱导来扩增TRAIL（肿瘤坏死因子相关的凋亡诱导配体）诱导的凋亡。该化合物的这些特征似乎与其抑制帽依赖性蛋白质翻译的能力无关，后者是由于通过与eIF4E结合而破坏eIF4E / eIF4G缔合而引起的。已经表明，尽管4EGI-1从eIF4E置换出eIF4G，但其却同时增强了体内和体外的4E-BP缔合。4E-BPs调节了eIF4E / eIF4G复合体，该复合体在翻译起始水平上对基因表达的调控中起着核 eIF4E/eIF4G Interaction Inhibitor, 4EGI-1, has been shown to amplify TRAIL (tumor necrosis factor-related apoptosis-inducing ligand)-induced apoptosis via down-regulation of FLIP|S/L|and induction of DR5. These characteristics of the compound seem to be independent of it′s ability to inhibit cap-dependent protein translation which is caused by disruption of the eIF4E/eIF4G association through binding to eIF4E. It has been shown that while 4EGI-1 displaces eIF4G from eIF4E, it consequentially enhances 4E-BP association both|in vivo|and|in vitro|. 4E-BPs regulated the eIF4E/eIF4G complex which has a central role in the regulation of gene expression at the level of translation initiation.