SETDB1 and prostate cancer: In addition, we found SOD1 expression can repress methylation in NSCLC, this consistent with findings that SOD1 knockdown induces oxidative stress and DNA methylation loss in prostate cancer (Bhusari et al., 2010), The underlying mechanism is likely that inhibition of reactive oxygen species (ROS) leads to an increase in SETDB1, as Park et al. (2019) reported that piperlongumine (Huang et al.)can downregulate SETDB1 to selectively kill breast cancer cells via accumulation of ROS, while the ROS inhibitor N-acetyl cysteine could recover the decrease in SETDB1 expression induced by PL.