This evidence indicates that metarrestin partly exerts its activity through interfering with the non-translational functions of eEF1A2, linking it mechanistically to other small-molecule inhibitors targeting eEF1A such as plitidepsin and didemnin B. However, unlike those compounds, metarrestin appears to selectively modulate nucleolar function and ribosome biogenesis without broadly suppressing global translation, offering a distinct therapeutic strategy for targeting metastatic cancer through eEF1A-dependent pathways. The gene discussed is EEF1A1; the disease is metastatic malignant neoplasm.