Specific genetic alterations (MKRN3, KISS1, KISS1R, DLK1, GPR54, and also other syndromes), central nervous system lesions (e.g., hypothalamic hamartoma) and social and environmental stressors (e.g., adoption or endocrine disruptors) are major drivers of CPP, although the majority of patients with CPP have no identified etiology and are labeled as idiopathic CPP. Here, KISS1R is linked to central precocious puberty.