Meningiomas are the most common primary brain tumors, accounting for 33.8% of all primary brain and central nervous system tumors in the U.S. between 2002 and 2006. They are generally benign but can be life-threatening due to their intracranial location. Genetic factors, such as mutations in the NF2 gene, and environmental factors like ionizing radiation are associated with increased risk. Hormonal factors, including endogenous and exogenous hormones, are also suspected due to the gender disparity in meningioma incidence and the presence of hormone receptors in these tumors. However, the exact etiology remains unclear, and research is ongoing. Epidemiological studies have shown that meningiomas are under-researched compared to malignant glial tumors. Challenges include the long latency period, recall bias, and subclinical disease prevalence. The Benign Brain Tumor Cancer Registries Amendment Act of 2002 improved reporting of meningioma incidence and survival. Prevalence estimates suggest around 97.5 per 100,000 in the U.S., with higher rates in women. Risk factors include ionizing radiation, hormonal use, and possibly genetic predisposition. However, the evidence for hormonal risk factors is inconsistent. Studies on ionizing radiation show increased risk, particularly in those exposed to high doses. Hormonal factors, such as oral contraceptives and hormone replacement therapy, have shown mixed results. Head trauma and cell phone use have also been investigated, but findings are inconclusive. Meningiomas are associated with breast cancer, possibly due to shared risk factors rather than a direct causal relationship. Occupational and dietary factors have not shown consistent associations. Family history of meningioma is linked to increased risk, particularly with NF2 mutations. Molecular studies suggest that meningiomas involve genetic and epigenetic changes, with NF2 deletions being common. However, the exact genetic mechanisms remain unclear. Future research should focus on large-scale studies, integrating environmental and genetic factors, and exploring the interaction between them. Improved epidemiological tools and genetic studies are needed to better understand meningioma etiology and risk factors. The field benefits from increased reporting and the use of genetic and molecular epidemiological tools to identify subtypes and risk factors. Collaborative efforts are essential to address the complex interplay between genetic susceptibility and environmental exposures in meningioma development.Meningiomas are the most common primary brain tumors, accounting for 33.8% of all primary brain and central nervous system tumors in the U.S. between 2002 and 2006. They are generally benign but can be life-threatening due to their intracranial location. Genetic factors, such as mutations in the NF2 gene, and environmental factors like ionizing radiation are associated with increased risk. Hormonal factors, including endogenous and exogenous hormones, are also suspected due to the gender disparity in meningioma incidence and the presence of hormone receptors in these tumors. However, the exact etiology remains unclear, and research is ongoing. Epidemiological studies have shown that meningiomas are under-researched compared to malignant glial tumors. Challenges include the long latency period, recall bias, and subclinical disease prevalence. The Benign Brain Tumor Cancer Registries Amendment Act of 2002 improved reporting of meningioma incidence and survival. Prevalence estimates suggest around 97.5 per 100,000 in the U.S., with higher rates in women. Risk factors include ionizing radiation, hormonal use, and possibly genetic predisposition. However, the evidence for hormonal risk factors is inconsistent. Studies on ionizing radiation show increased risk, particularly in those exposed to high doses. Hormonal factors, such as oral contraceptives and hormone replacement therapy, have shown mixed results. Head trauma and cell phone use have also been investigated, but findings are inconclusive. Meningiomas are associated with breast cancer, possibly due to shared risk factors rather than a direct causal relationship. Occupational and dietary factors have not shown consistent associations. Family history of meningioma is linked to increased risk, particularly with NF2 mutations. Molecular studies suggest that meningiomas involve genetic and epigenetic changes, with NF2 deletions being common. However, the exact genetic mechanisms remain unclear. Future research should focus on large-scale studies, integrating environmental and genetic factors, and exploring the interaction between them. Improved epidemiological tools and genetic studies are needed to better understand meningioma etiology and risk factors. The field benefits from increased reporting and the use of genetic and molecular epidemiological tools to identify subtypes and risk factors. Collaborative efforts are essential to address the complex interplay between genetic susceptibility and environmental exposures in meningioma development.