IFNA1 and systemic lupus erythematosus: In view of our results, we hypothesize that a potential mechanism by which IFNα could increase CV risk may be by promoting a premature EPC differentiation, generating mEPC (CD133−) with little or no vasculogenic and/or repair capability [6], probably similar to the “non-angiogenic phenotype” reported in murine SLE models [16], consequently resulting in a defective EPC-mediated endothelial repair.