In summary, we revealed the pathogenic relationships among NR4A1, c-Fos and PRDX6 in patients with BC and demonstrated a functional network in which the NR4A1–c-Fos interaction inhibits c-Fos-mediated transcriptional control of lipid remodeling and redox dyshomeostasis in BC (Fig. 8f). The gene discussed is FOS; the disease is breast cancer.