DNMT1 and cancer: Despite this, the lack of significant differences in DNA methylation between M1 and M2 macrophages in our dataset and the fact that DNMT inhibitor activity depends on their integration into the genome of highly proliferative cells such as cancer cells [70, 71] and not in less proliferative macrophages [72–75], suggest that DNMT inhibitors may not be the most effective epigenetic drug for macrophage modulation.