In contrast, Lundström et al. also reported that all SE alleles tested (*01, *04:01, *04:04, *04:05, *04:08, and *10:01) strongly interacted with CS in conferring an increased risk of ACPA-positive RA, regardless of the fine specificity of SE in the EIRA cohort (1319 cases and 943 controls) [129]. Here, PRTN3 is linked to rheumatoid arthritis.