The growth of VS may cause sensorineural hearing loss, tinnitus, facial palsy, deafness, brainstem compression, and eventual mortality.[2] So far, the identification of the NF2 gene in 1993 has been the most important contribution to our understanding of VS pathogenesis,[3] but it is likely that other genes contribute to VS formation because the NF2 gene is intact in a significant proportion of cases.[4] To date, the pathologic mechanisms leading to VS have not been fully elucidated, new therapeutic targets for VS are desperately needed. Here, NF2 is linked to sensorineural hearing loss disorder.