TNFAIP3 and non-Hodgkin lymphoma: On this basis, genetic variants of genes implicated in the regulation of chronic inflammation such as TNFAIP3 [12]–, [14] and LILRA3 [15], B cell activation [16], [17], type I IFN pathways such as TREX-1 [18] as well as epigenetic processes [19] have been shown to increase the risk of Non-Hodgkin Lymphoma (NHL) in SS.