MKI67 and meningioma: Finally, although we investigated possible factors that could contribute to abnormal CDKN2A expression, there may be additional, less common alterations in meningiomas that impact shared pathways, such as CDKN2C alterations, BAP1 loss, TP53 mutations/deletions, and/or MDM2 amplifications that mandate further exploration and correlation with other histopathological features (e.g. mitoses, Ki-67, brain invasion, other atypical features) in order to extend the scope of our findings [4, 9, 47].