IFNA1 and systemic lupus erythematosus: This would explain the reason why only a minor fraction of IFNα-treated patients succumb from SLE [76,77,78,79,80], why only lupus-prone mice, but not mice without genetic predisposition to autoimmunity, develop SLE upon continuous exposure to high amounts of IFNα [81,82,83], and why type I IFNα sometimes showed protective effects on SLE [73,74].