Using the pancreatic islets of Wistar rat offspring and analyzing them with bisulfite sequencing to find patterns in the DNA methylation of CpGs in the promoter regions of cyclin-dependent kinase inhibitor 2A/B (Cdkn2A/B), the methylation level of the Cdkn2A promoter was lower in the GDM-exposed offspring, implying that this effect could alter epigenomic characteristics in the Langerhans islets by causing decreased β-cell mass proliferation and mild hyperglycemia, which could be the origin of diabetes (Figure 2) [80]. This evidence concerns the gene CDKN2A and Hyperglycemia.