It has been documented that BI in meningioma is correlated to molecular alterations at various cellular components and in signal transmission pathways, and alterations in metalloproteases, particularly MMP-9 [26], adhesion molecules deficits, the role of the tumor microenvironment and glial cells, growth factors, and mitotic index, appear to contribute to the pathogenesis of brain infiltration [16,58,59]. Here, CACNA1A is linked to neoplasm.