Longer telomeres in DS children could be explained by having reduced cellular proliferation during embryonic development, as demonstrated by lower Ki67 and cyclin A levels in DS animal fetuses, compared to the control group [13], but they could also have multiple explanations such as advanced parental age at conception, comorbidities which slow down telomere shortening, such as hypothyroidism, autoimmune disorders, or hormonal imbalances, due to the lowered proliferation of lymphocytes, which might result in a protective action on telomere length [14]. This evidence concerns the gene MKI67 and Dravet syndrome.