In this case, autoantibodies and IFNα in the serum of SLE patients suppress glutathione peroxidase 4 (GPX4) expression through the calcium/calmodulin kinase IV (CaMKIV)/cAMP response element modulator (CREM)α signaling axis, thereby enhancing the production of lipid-ROS to induce ferroptosis, a major form of neutrophil cell death during SLE.[26]. This evidence concerns the gene CAMK4 and systemic lupus erythematosus.