The association between Ro52/TRIM21 and other proteins such as TRIB2, implicated in driving tumorigenesis [43], with Fas-associated death domain (FADD) and negatively regulating the IFN-α pathway in response to viral infection [44] and its interaction with virus-like particles and high-affinity IgG receptors affecting the intracellular fate of viruses, including degradation by the proteasomes [10,45,46] may provide important insights into the generation of the autoantibody response and its perpetuation in SSc. This evidence concerns the gene IFNA1 and viral infectious disease.