Nevertheless, among post-COVID-19 patients, the anti-cyclic citrullinated protein (CCP) antibody, or ACPA, a hallmark autoantibody in RA, did not show any significant differences between the patients with and without arthritis (89); therefore, cytokine dysregulation, rather than antibody-mediated responses, may play a role in the occurrence of RA following COVID-19 (82), (89). This evidence concerns the gene PRTN3 and rheumatoid arthritis.