Geoffrey Harris in his renowned 1955 monograph suggested “a major factor responsible for puberty is an increased rate of release of pituitary gonadotrophin” and “that a neural (hypothalamic) stimulus, via the hypophysial portal vessels, may be involved.” It is now known that this hypothalamic stimulus is gonadotropin releasing hormone (GnRH), and that pulsatile GnRH secretion is essential for puberty. Contemporary models of GnRH pulse generation posit that a subset of cells in the arcuate nucleus co-expressing kisspeptin, neurokinin B and dynorphin are a critical component. As Harris recognized, the postnatal delay to puberty cannot be accounted for by “immaturity” of either gonads or pituitary because if these glands of the juvenile are provided with an adult gonadotropic or hypophysiotropic stimulus, respectively, post-pubertal function is initiated precociously. An analogous strategy applied to the monkey indicates that GnRH neurons are also non-limiting to the onset of puberty in primates. So what is responsible for the delay of puberty? In Old-World monkeys and man, in which the delay is prolonged, a neurobiological brake is imposed upon the GnRH pulse generator from late infancy until termination of the juvenile phase of development. The brake’s cellular and molecular components and its genetic underpinnings are poorly understood, as are those of the control system that times the application and withdrawal of the brake. With regard to the latter, a central neural growth-tracking device, termed a somatometer, has been proposed to account for co-ordination between release of the brake and attainment of approaching adult body size. The timing and tempo of puberty may be influenced by prenatal environment, post-natal nutrition, and psychosocial factors but how these modulators interface with the core hypothalamic components governing the onset of this critical phase of development, and roles played by epigenetics in this regard are only beginning to emerge.