It was confirmed that the damage of A20 protein encoded by TNFAIP3 leading to impaired control of NF‐κB activation in B cells continuously stimulated by autoimmunity enhanced the risk of lymphoma.25 In the analysis of autoimmune conditions and the risk of NHL and subtypes, SS and systemic lupus erythematosus were shown to be associated with a 30‐fold and eightfold increased risk of marginal zone lymphoma, respectively, and there was a 1000‐fold increase in the risk of parotid gland MALT lymphoma among SS patients. This evidence concerns the gene TNFAIP3 and systemic lupus erythematosus.