In addition to the above findings, the majority of them were involved in a number of potentially interesting pathways such as scavenging heme from plasma, platelet activation, acute-phase responses, degranulation, signaling, aggregation, and the creation of C4 and C2 activators, etc. These pathways are highly relevant to the present study since SLE is an autoimmune disease caused by abnormalities that affect the immune system and in turn cause an acute inflammatory response. The gene discussed is C2; the disease is autoimmune disease.