Additionally, modulation of PP2A carboxymethylation has been studied in the context of cancer therapeutic response, where overexpression of PME-1 was found to drive kinase inhibitor resistance in glioma cells and knockdown of PME-1 increased sensitivity to epidermal growth factor receptor (EGFR) and Polo-Like Kinase 1 (PLK1) inhibitors in lung adenocarcinoma cells (93). Here, PLK1 is linked to lung adenocarcinoma.