Notably, ferroptosis of neutrophils has been documented in patients with SLE.[178] In patients with SLE, autoantibodies and IFN‐α augment ferroptosis in neutrophils by intensifying the binding of the transcription suppressor CREMα to GPX4 promoters through activation of calcium/calmodulin kinase IV (CaMK IV), thereby reducing GPX4 expression and subsequently amplifying lipid ROS (Figure 7). This evidence concerns the gene CAMK4 and systemic lupus erythematosus.