For example, fewer STING protein molecules accumulate on the Golgi (by microscopy) in Gcc2-deficient cells than Copa-deficient cells; this correlates with in vivo phenotypes – Gcc2-deficient mice only develop moderate serological autoimmunity with no tissue pathology or immune cell dysregulation, whereas Copa-deficient mice have much more severe disease7. This evidence concerns the gene STING1 and Autoimmunity.