The underpinning reasons for the manifestation of the typical phenotypic features especially the endocrine disturbances in DS (hirsutism and hypertrichosis)—encountered also in our patient and usually observed in almost all cases of DS—might be explained by the reduction of sex hormone-binding globulin provoked by insulin action via the type 1 insulin-like growth factor (1 IGF) receptor, which has functional and structural similarities with the insulin receptor.20 This evidence concerns the gene SHBG and hypertrichosis.