Downregulation of AMH expression by androgens, through AR interaction with the transactivating factor SF129, underlies the decrease of serum AMH in both normal and precocious puberty in males26, whereas the lack of AR expression in the fetal and early infantile Sertoli cells31–33 explains why AMH remains high in spite of intratesticular androgen concentrations similar to those seen in adults and in boys with precocious puberty diagnosed before the age of 1 year34. Here, AMH is linked to precocious puberty.