Sexual precocity results from both GnRH-dependent and GnRH-independent mechanisms. The GnRH-dependent forms of precocious puberty can be treated effectively with long-acting agonist analogues of GnRH. However, for some children who have a poor growth rate during the analogue therapy, an additional growth hormone therapy should be considered to get them near to their normal final height. The analogue treatment could be continued until a bone age of 13 or more. The GnRH-independent forms of precocious puberty have unique mechanisms and unknown pathophysiology. For instance, even though it is known that testotoxicosis and McCune Albright syndrome are caused by the molecular mechanism disorders, further elucidation of their etiologic basis of sexual precocity is needed. Thus being, in treating the GnRH-independent forms they should be assessed for each particular disorder.