In view of the fact that MyD88 is a central mediator in TLR 7 and 9 signaling, these inhibitors of MyD88 dimerization and recruitment of essential kinases could prove to be an effective treatment option in lupus by abolishing the aberrant TLR signaling that induces the elevated type I IFN levels and persistent inflammation. The gene discussed is MYD88; the disease is systemic lupus erythematosus.