In agreement with these observations, and supported by preclinical observations that specific IFN-α inhibitors improve murine SLE [29], the development of tailored therapeutic approaches aimed at specifically inhibiting the function of IFN-α with monoclonal antibodies, anti-IFN-α receptor antibodies, IFN-α-kinoid, or downstream small molecules, targeting the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathways, are being considered in clinical trials for SLE patients [5]. The gene discussed is SOAT1; the disease is systemic lupus erythematosus.