Additionally, non-traditional risk factors derived from the SLE pathophysiology, such as the glucocorticoid treatment, and inflammatory mediators such as type 1 interferons (IFN), tumor necrosis factor-alpha (TNF-α), and C-reactive protein (CRP) are involved in CVD development [4,5,6]. The gene discussed is IFNA1; the disease is systemic lupus erythematosus.