We suggest that the cytoplasmic release of DNA from FRA9A-enhanced MN, may further tip the balance by exacerbating the stimulation of the aberrantly hyperactive cGAS-STING initiated IFN expression in C9orf72Exp carriers (4,13,14), which may explain the co-morbid partially-penetrant autoimmunity (1–6). The gene discussed is IFNA1; the disease is Autoimmunity.