Such glial ERK signaling drives normal synaptic pruning, and a Noonan Syndrome patient-derived protein tyrosine phosphatase non-receptor type 11 (PTPN11) mutation within glia increases ERK signaling to exacerbate experience-dependent synaptic pruning (Baumann et al., 2024). The gene discussed is PTPN11; the disease is Noonan syndrome.