Schuster et al. utilized a lentiviral knock-down (KD) technique in the non-obese diabetic (NOD) mice model to demonstrate that inhibiting CLEC16A via silencing can protect against autoimmunity in T1D, which stands in contrast to the increased susceptibility to autoimmunity caused by reducing the expression of CLEC16A. This evidence concerns the gene CLEC16A and type 1 diabetes mellitus.