Interestingly, the majority of RGNT have at least two, and often three, different pathogenic mutations involving FGFR1, either PIK3CA or PIK3R1, and often also NF1 or PTPN11. As such, genetic activation of both the Ras-Raf-MEK-ERK and PI3-kinase-Akt-mTOR signaling pathways appears to be fundamental to the pathogenesis of RGNT. The gene discussed is AKT1; the disease is rosette-forming glioneuronal tumor of fourth ventricule.