These findings point again to the heterogeneity in the pathogenesis of SLE and that a better definition of disease subsets could be necessary for this kind of studies to be able to determine the possible role of decreased SOCS1 in constitutive Jak1 and STAT2 phosphorylation in SLE and whether the two possible groups observed by these means behave differently. This evidence concerns the gene STAT2 and systemic lupus erythematosus.