Several genetic and environmental factors have been implicated in SLE etiopathogenesis, but in recent years increased type I interferon (IFN-I, IFNα and IFNβ) expression has been discovered to play a key role in the majority of SLE patients, despite being known for over 30 years that it is elevated in SLE patients[1-4]. Here, IFNA2 is linked to systemic lupus erythematosus.