The underlying genetic mutations induce an accumulation of DNA and RNA fragments, generated during the genomic repair process, which act as a trigger for the production of IFN I. Other pathologies, such as systemic lupus erythematosus (SLE) have in common with the interferonopathies the overproduction of IFN and skin involvement. The gene discussed is IFNA1; the disease is systemic lupus erythematosus.