Crosstalk between cancer cells and TAMs in the TME can also activate NRF2 in TAMs to reshape the tumor immune microenvironment via multiple mechanisms including suppression of pro-inflammatory cytokines, increasing expression of PD-L1, macrophage colony-stimulating factor (M-CSF) and KYNU, and accelerating catabolism of cytotoxic-labile heme (185). The gene discussed is CSF1; the disease is neoplasm.