The nature of Systemic Lupus Erythematosus (SLE) involves a complex network of uncontrolled activations of signals, which leads to a vast range of symptoms. SLE is an autoimmune disease that manifests itself when the immune system attacks the body’s cells and tissues, resulting in inflammations in joints, organs, and skin. The course of the disease is unpredictable and much more is to be understood about the mechanisms of the illness and the background of the patients who are prone to the disease. This study explores both the mechanistic and clinical aspect of SLE in an attempt to gain a broader view of the disease. Using 3 interferon stimulated genes, MX1, PKR, and CXCL10, we evaluated interferon scores of 66 patients. We then utilized cluster analysis to divide patients into two main groups based on interferon scores: Group 1 consisted of controls and SLE patients with low interferon scores (0.4), Group 2 consisted of SLE patients with high interferon scores (10.4). These groups were compared with interferon stimulated genes, RNase1 and Toll-Like Receptors 7 (TLR7), which positively correlated with interferon scores. A system called Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) is often utilized to quantitatively assess patients’ disease activity. The criteria in the evaluation of patients included symptoms often associated with SLE. The score in SLEDAI reflected the disease activity of the patient. In this study, we investigated the relationship between SLEDAI and interferon score, in which we found no correlation. However, when we examined Group 2, there was a trend towards better correlation with SLEDAI. In the clinical aspect, we examined age, race, and gender of SLE patients. In addition, we collected information on autoantibody titers such as double stranded DNA (dsDNA), antiphospholipid antibodies, and antinuclear antibodies (ANA), all of which may be important indicators of disease activity.