According to the existing theories and our analysis, the possible mechanism of the susceptibility to DLBCL in RA patients is that LGALS2 causes persistent chronic inflammation and excessive activation of B cells through the production of many inflammatory factors and autoantibodies, thus leading to the occurrence of DLBCL (7), which also supported by previous studies reporting a strong relationship between lymphoma incidence and RA disease severity (43, 44). This evidence concerns the gene LGALS2 and diffuse large B-cell lymphoma.