Recent reports of humans who have normosmic idiopathic hypogonadotropic hypogonadism due to TAC3 or TACR3 (encoding neurokinin B and its receptor, NK3R, respectively) mutations provided compelling evidence for the involvement of neurokinin B (NKB) signaling in puberty. This apparently stimulated the field to understand the exact mechanism through which NKB signaling exerts its effects. With the important findings from these recent studies a sketch of GnRH pulse generator has emerged in which NKB signaling appears to play a key role. In this communication, NKB involvement in puberty is reviewed from the perspective of the fundamental question of "what controls puberty?" (C) 2010 Elsevier Ireland Ltd. All rights reserved.