Hsu et al. identified a non-canonical MET activity of etoposide, which suppresses the EMT/β-catenin/PD-L1 axis through TOP2B degradation-dependent nuclear β-catenin reduction, leading to PD-L1 downregulation of CSCs and non-CSCs and sensitization of cancer cells to anti-Tim-3 therapy 43. The gene discussed is TOP2B; the disease is cancer.