Consistently, increased nuclear accumulation and enhanced binding of CREMα on the GPX4 promoter were observed in SLE neutrophils or healthy neutrophils cultured with SLE serum, IgG or IFN-α, compared with control neutrophils; further, genetic knockdown of CREMα reversed GPX4 expression suppression by IgG or IFN-α, while CREMα overexpression reduced GPX4 expression. This evidence concerns the gene IFNA1 and systemic lupus erythematosus.