Considering that the dephosphorylation of AURKB substrates by PP2A phosphatase is the upstream factor that silences the AURKB signal (28), we wondered whether treatment with the PP2A inhibitors (PP2Ais) could reactivate AURKB in BRCA2/NSFL1C double-silenced cells, which can simulate BRCA2 defect tumor cell death as a result of SAC activation. This evidence concerns the gene PTPA and neoplasm.