Recent studies have suggested that IgG4-RD presents with a range of tissue phenotypes, progressing from a proliferative (inflammatory) to fibrotic phase.[17] This balance may depend on the activities of infiltrating CD4 + and CD8 + T cells and B cells as well as fibroblasts that orchestrate fibrosis.[18] It is plausible that diabetes-related immunosuppression may disrupt this balance, leading to a chronic abscess organized via fibrosis. This evidence concerns the gene CD4 and immunoglobulin G4-related sclerosing disease.