Both the prevalences and the titres of the anti–type I IFN autoantibodies are higher in APS1 patients than in MG/thymoma patients [10,11]; they are also far higher—and much broader in IFN-α subtype cross-reactivity—than those of antibodies induced by therapy with IFN-α [43,44]. The gene discussed is IFNA1; the disease is myasthenia gravis.