Molecular profiling efforts of sporadic benign meningiomas have identified two, large, molecularly and clinically divergent clusters: a clinically heterogeneous group of tumors with mutations of the NF2 gene and/or loss of chromosome 22; and non-NF2 meningiomas with frequent alterations in the Sonic hedgehog (Shh) pathway, phosphatidylinositol-3-kinase (PI3K) signaling pathway, and TRAF7, KLF4, or POLR2A genes, which are clinically benign and often occur at the base of the skull [11-13]. This evidence concerns the gene NF2 and benign meningioma.