Della Torre et al. [14] found that increased serum IgE and eosinophil levels are independent of atopic disease history, revealing that these factors reflect mechanisms inherent to the immune response driving IgG4-RD; they also found that T-helper type 2 (Th2) cells play crucial roles in IgG4-RD pathogenesis [14] and proved that the IgG4-RD Th2-polarized immune state is related to antecedent atopic disease rather than disease activity [28]. This evidence concerns the gene IGHE and immunoglobulin G4-related sclerosing disease.