Machen et al. engineered an oligodeoxynucleotide antisense (AS-ODN) that targets the transcription of CD80 and CD86 in BMDCs, leading to the inhibition of NO, TNF-α, and IL-12 secretion [57] and a delayed onset of type 1 diabetes (T1D) in NOD mice. This evidence concerns the gene CD80 and type 1 diabetes mellitus.