Treatment with the anti-DLL4 antibody in spontaneous humanized T1D mice helps in amplifying antigen-specific Treg cell proliferation in the thymus, peri-pancreatic lymph nodes, pancreases, and spleen, which consecutively enriches peripheral GAD65-antigen-specific Treg cell population as reported previously in NOD mice (Billiard et al., 2012, 2018). This evidence concerns the gene GAD2 and type 1 diabetes mellitus.