To review our current understanding of the molecular pathogenesis of meningiomas, to suggest topics for future investigations, and to present perspectives for clinical application. Significant progress has been made in recent years in delineating the molecular mechanisms involved in meningioma formation, growth, and malignant progression. However, many questions remain unanswered. Mutations in the NF2 gene probably account for the formation of more than half of all meningiomas. On the other hand, the molecular events underlying the initiation of meningiomas without NF2 mutations have yet to be identified. Investigating hereditary conditions associated with an increased meningioma incidence and the mechanisms underlying the development of radiation-induced meningiomas could potentially yield relevant insights. Meningioma growth is sustained by the dysregulated expression of steroid hormones, growth factors, their receptors, and activation of signal transduction cascades. The underlying genetic causes are unknown. Malignant progression of meningiomas probably involves the inactivation of tumor suppressor genes on chromosomes 1p, 9p, 10q, and 14q. However, with the possible exception of INK4A/INK4B, the actual targets of these chromosomal losses have remained largely elusive. Cell cycle dysregulation and telomerase activation have been recognized as important steps in meningioma progression. Telomere dynamics, cell cycle control, and the mechanisms responsible for deoxyribonucleic acid damage control are tightly interwoven. Investigating genes involved in the maintenance of genomic integrity might significantly deepen the understanding of meningioma progression. An area that has received relatively little attention thus far is the genetic background of meningioma spread and invasion. Possible clinical applications of the molecular data available may include a meningioma grading system based on genetic alterations, as well as therapeutic strategies for refractory meningiomas aimed at interfering with signal transduction pathways.