Theseresults suggest that a loss of methylation and overexpressionof these cell cycle inhibitory genes possibly increase thesusceptibility of type 2 diabetes through an inhibited cyclinD1-CDK4 complex formation, leading to a decreased β-cellmass and mild hyperglycemia in the GDM-exposed offspring.Meanwhile, further investigations and larger-sclae studies areneeded to completely investigate the molecular process ofinducing diabetes in the offspring by GDM. The gene discussed is CDK4; the disease is type 2 diabetes mellitus.