Opposite to that reducing cholesterol biosynthesis flux could enhance IFN‐I and ISGs expression in macrophages,[12] our previous study revealed that the accumulation of the cholesterol precursor 7‐dehydrocholesterol (7‐DHC) could promote IFN‐I production in macrophages against viral infection.[13] Consequently, it is crucial to identify which cholesterol metabolites are abnormally produced and are functionally linked with IFN and ISGs to control the pathogenesis of SLE. This evidence concerns the gene IFNA1 and systemic lupus erythematosus.