INS and type 1 diabetes mellitus: There is evidence of augmentation in the T1DM risk through the mechanisms of genomic imprinting with the participation of the INS gene [10] and the alternative splicing of islet cell autoantigen IA-2 mRNA [11], as well as through gene–gene and gene–environment interactions stipulated by epigenetic modifications [12,13] or retrovirus-mediated changes in different cells involved in pancreatic β-cell functioning [14,15].