In systemic lupus erythematosus (SLE), activation of the cGAS-STING pathway exacerbates disease phenotype through multiple mechanisms, including induction of hyperactivation of the complement system, and production of inflammatory molecules such as type I interferons (IFN-α and IFN-β), TNF-α, and interleukins (IL-6 and IL-1) (Feng et al., 2024; Troldborg et al., 2018). This evidence concerns the gene IFNA1 and systemic lupus erythematosus.