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. 2020 Feb 14;52(2):192–203. doi: 10.1038/s12276-020-0384-2

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — The first approach is based on lowering ROS levels to counteract their role in cellular transformation; it is aimed at reducing the number of transformed cells by depriving them of fuel (represented in the upper right side of the figure as a lower proportion of transformed cells with respect to that of normal cells). The second approach is based on the consideration that cancer cells, with an antioxidant system already triggered, are more sensitive than their normal counterparts to further increases in ROS and are unable to achieve redox balance. Therefore, by inducing ROS under these metabolic conditions, a high percentage of the cells undergo death (represented in the lower right side of the figure, where transformed cells are depicted as apoptotic).