As expected, β-catenin knockdown, similar to etoposide, suppressed STT3 and PD-L1 in mesenchymal cancer cells (Fig. 8h, lanes 2 and 3) and rendered cells insensitive to etoposide or sg-TOP2B treatment (Fig. 8h, lanes 4 and 8), supporting the notion that etoposide-mediated TOP2B degradation and subsequent inhibition of the EMT/β-catenin/STT3/PD-L1 axis is likely through downregulation of nuclear β-catenin. This evidence concerns the gene TOP2B and cancer.