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. 2018 Feb 20;9(3):294. doi: 10.1038/s41419-018-0268-8

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© The Author(s) 2018

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. 1 — NDRG2 expression in TAMs facilitates their M2-like polarization (green). This results in the production of interleukin-10 (IL10), the promotion of a tumor-supportive microenvironment and tumor growth. The absence of NDRG2 in TAMs (red) in turn favors M1 polarization, production of IL12, IL1β and tumor necrosis factor-α (TNFα) and the suppression of tumor growth