In a meta-analysis, non-HLA factors, including polymorphism within insulin variable number of tandem repeats (INS-VNTR), protein tyrosine phosphatase non-receptor type 22 (PTPN22), cytotoxic T-lymphocyte associated protein 4 (CTLA4), interleukin-2 receptor subunit alpha (IL2RA), and increased T cell activation and proliferation contribute to the pathogenesis of T1DM [15,16,17,18]. The gene discussed is INS; the disease is type 1 diabetes mellitus.