The mechanistic insights revealed that the stable knockdown of SETD7 significantly impaired the cell proliferation and viability in MCF-7 and MDA-MB-231 breast cancer cells, also leading to an increased intracellular ROS content and a decreased GSH/GSSG ratio due to the repression of NRF2-dependent antioxidant genes expression. The gene discussed is SETD7; the disease is breast carcinoma.