Most recently, studies have demonstrated that loss of Mkrn3 expression leads to an increase in dendritic spines in the arcuate nucleus, which has a role in regulating neuronal development and plasticity.[40] Multiple nonsense, missense, and copy number variants in MKRN3 have been identified in children with CPP, with a median age of onset of puberty in girls six years of age.[41, 42] It is reported that MKRN3 variants associated with CPP are not linked to cognitive impairment.[42]. The gene discussed is MKRN3; the disease is Cognitive impairment.