Our comparison of insect and human cancer cell proline oxidation confirmed that while PRODH can induce mitochondrial ROS production, it does so by respiratory chain stimulation and not as a direct product of inner membrane PRODH enzymatic activity (Goncalves et al. 2014), supporting the concept that cancer cell context likely determines PRODH’s pivotal role as either a ROS-inducing tumor suppressor or an ATP-generating growth and survival mechanism. Here, PRODH is linked to neoplasm.