This, together with the observation that NF2 mutations were always present in heterozygosis, could suggest that mutations of the NF2 gene could be a secondary event in the development of meningiomas which would occur after the loss of chromosome 22 and that therefore, inactivation of other genes coded in chromosome 22 (e.g. SMARCB1[33]) could potentially play a major role in tumor development, even among NF2 mutated cases. This evidence concerns the gene NF2 and meningioma.