Numerous data from the animal models treated with synthetic dsRNA analogue, polyinosinic–polycytidylic acid [poly(I:C)], support the hypothesis that disturbed TLR3 function may contribute to the development of T1D in susceptible individuals (Alkanani et al. 2014; Devendra et al. 2005; Moriyama et al. 2002; Sobel et al. 1992). This evidence concerns the gene TLR3 and type 1 diabetes mellitus.