Considering the high penetrance of mutations of MKRN3 as a cause of genetic forms of central precocious puberty [10,11,31,32] and the presence of three evolutionarily conserved binding sites for miR-30 family members in the 3′ UTR of MKRN3, our data pave the way for specific analyses of the potential pathogenic role of deregulated miR-30/MKRN3 in pubertal disorders in humans. The gene discussed is MKRN3; the disease is central precocious puberty.