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A major difficulty in the genetic study of type 1 diabetes (T1D) is the lack of means to identify candidate disease genes, as the exact disease etiology is still unclear. We have developed a minimal model for T1D where we mathematically formulate the population dynamics for the most critical components in β-cell destruction: macrophages, T lymphocytes, β cells and β-cell autoantigens. System dynamic stability analysis revealed that the disease process for adult individuals is critically regulated by several major gene regulation pathways. Together they provide a comprehensive picture of where the candidate genes most likely lie. We will present our model, our bioinformatics platform to retrieve and update the gene information involved in the pathways, and our candidate gene database. In addition we will present our plan of candidate gene genotyping. Our approach represents the first time understanding the disease dynamics is integrated with the genetic study of a complex disease.