In this thematic context, we found that NRF2 activation represses immunosuppressive cytokine signaling mediated by IL-10 and TGFβ, which will function to repolarize myeloid-derived cells away from the tumour promoting M2-lineages, and therefore together, the available data support a model in which NRF2 inducers broadly reprogram the tumour microenvironment towards an anti-cancer phenotype by reversing the immunosuppressive functions of regulatory cells within the tumour niche. Here, TGFB1 is linked to neoplasm.