Current research stratifies RA phenotypes based on serological antibodies—rheumatoid factor (RF) or ACPA—into seropositive RA (SPRA, positive for RF and/or ACPA) or seronegative RA (SNRA, negative for both RF and ACPA), each typically associated with distinct genetic susceptibilities and immunopathogenic pathways [17,18]. This evidence concerns the gene PRTN3 and rheumatoid arthritis.