CD8A and type 1 diabetes mellitus: Rather, they can establish robust mechanisms to mitigate the autoimmune attack.71 Somewhat counterintuitively, these also include the hyper-expression of MHC-I since β-cells express not only classical molecules involved in CD8+ T-cell activation but they also upregulate “non-classical” MHC-I molecules which can resist immune-mediated attack.71 Molecules such as MHC-E, F, and G become hyper-expressed on β-cells in type 1 diabetes and can engage influent innate immune cells to down-regulate their cytotoxicity.