Contrastingly, RNAi-mediated PON2 knockdown was found to further elevate the rates of apoptosis and imatinib susceptibility (Witte et al. 2011) while PON2-deficient lung adenocarcinoma cells caused concentration-dependent surges in cell death and activation of caspase-3/7 upon C12 treatment (Whitt et al. 2023). This evidence concerns the gene PON2 and lung adenocarcinoma.