NRF1 and neoplasm: In in vitro experiments, CTCs formed clusters with PMN-MDSC and induced their pro-tumor differentiation via the paracrine nodal signal Nodal, which increased the production of reactive oxygen species (ROS) by PMN-MDSCs, and ROS upregulated Notch2 receptor expression in CTCs via the ROS-NRF1-ARE axis to promote tumor cell growth [101].