As a result of the plummeting activity of sex hormone-binding globulin by insulin action via the type (1 IGF) receptor, augmentation levels of the free circulating androgen (hyperandrogenism) are observed causing the endocrine disturbances in DS regardless of moderately high level of androstenedione, intact level of testosterone and feeble activity of androgens.21–23. This evidence concerns the gene SHBG and Dravet syndrome.