These genetic elements are involved in autoimmune diseases through various mechanisms, including molecular mimicry, whereby HERV-encoded proteins share epitopes with self-antigens, such as HERV-K10 MAG1 with IgG1 or HERV-W env with myelin, triggering cross-reactive responses (59), and the immune dysregulation caused by aberrant HERV expression, which disrupts T-cell tolerance and promotes autoantibody production, as seen in rheumatoid arthritis and lupus (60). This evidence concerns the gene GPAT3 and autoimmune disease.