Interestingly, the IFN-γ+HC subject (HC27) also had serum antibodies specific for Sm (a subunit of the U1-snRNP, using 5 SD cutoff) and for both Ro60 and La (using a 3 SD cutoff), suggesting this “healthy” subject is in preclinical evolution toward developing SLE, a disease in which we have previously described multiple different ACA including anti-IFN-α and anti-B cell-activating factor (BAFF)18. This evidence concerns the gene TNFSF13B and systemic lupus erythematosus.