There are several known causes for cavernous hemangiomas, but some cases are still unknown.
Radiation treatment used for other medical conditions has been suggested to cause cavernous malformation in some patients.

Hemangioma tumors are a result of rapid proliferation of endothelial cells and pericytic hyperplasia, or the enlargement of tissue as a result of abnormal cell division pericytes.
The pathogenesis of hemangioma is still not understood.
It has been suggested that growth factors and hormonal influences contribute to the abnormal cell proliferation.
Cavernous liver hemangiomas are more commonly diagnosed in women who have been pregnant.
As a result of this, it is believed that estrogen levels may play a role in the incidence of liver cavernomas.

Genetic studies show that specific gene mutations or deletions are causes for the disease.
The genes identified for cerebral cavernous hemangiomas (or malformations), are CCM1 (also KRIT1), CCM2 (also MGC4607, malcavernin) and CCM3 (also PDCD10).
The loss of function of these genes is believed to be responsible for cerebral cavernous malformations.
Furthermore, it is also believed that a "second hit mutation" is necessary for the onset of the disease.
This means that having a mutation in one of the two genes present on a chromosome is not enough to cause the cavernous malformation, but mutation of both alleles would cause the malformation.
Additionally, research on hemangiomas in general has shown that loss of heterozygosity is common in tissue where hemangioma develops.
This would confirm that more than a single allele mutation is needed for the abnormal cell proliferation.
KRIT1 has been shown to act as a transcription factor in the development of arterial blood vessels in mice.
CCM2 has overlapping structure with CCM1 (KRIT1) and acts as a scaffolding protein when expressed.
Both genes are involved with MAP3K3 and thus appear to be a part of the same pathway.

 CCM2 has been shown to cause embryonic death in mice.
Lastly, the CCM3 gene has been shown to have similar expression to CCM1 and CCM2, suggesting a link in its functionality.
Currently, no experiments have determined its exact function.
The lack of function of these genes in control of a proliferative signaling pathway would result in uncontrolled proliferation and the development of a tumor.
In 2018, it was theorized that proliferation of endothelial cells with dysfunctional tight junctions, that are under increased endothelial stress from elevated venous pressure provides the pathophysiological basis for cavernous hemangioma development.
There are several known causes for cavernous hemangiomas, but some cases are still unknown. Radiation treatment used for other medical conditions has been suggested to cause cavernous malformation in some patients.
Hemangioma tumors are a result of rapid proliferation of endothelial cells and pericytic hyperplasia, or the enlargement of tissue as a result of abnormal cell division pericytes. The pathogenesis of hemangioma is still not understood. It has been suggested that growth factors and hormonal influences contribute to the abnormal cell proliferation. Cavernous liver hemangiomas are more commonly diagnosed in women who have been pregnant. As a result of this, it is believed that estrogen levels may play a role in the incidence of liver cavernomas. 
Genetic studies show that specific gene mutations or deletions are causes for the disease. The genes identified for cerebral cavernous hemangiomas (or malformations), are CCM1 (also KRIT1), CCM2 (also MGC4607, malcavernin) and CCM3 (also PDCD10). The loss of function of these genes is believed to be responsible for cerebral cavernous malformations. Furthermore, it is also believed that a "second hit mutation" is necessary for the onset of the disease. This means that having a mutation in one of the two genes present on a chromosome is not enough to cause the cavernous malformation, but mutation of both alleles would cause the malformation. Additionally, research on hemangiomas in general has shown that loss of heterozygosity is common in tissue where hemangioma develops. This would confirm that more than a single allele mutation is needed for the abnormal cell proliferation. KRIT1 has been shown to act as a transcription factor in the development of arterial blood vessels in mice. CCM2 has overlapping structure with CCM1 (KRIT1) and acts as a scaffolding protein when expressed. Both genes are involved with MAP3K3 and thus appear to be a part of the same pathway. 
 CCM2 has been shown to cause embryonic death in mice. Lastly, the CCM3 gene has been shown to have similar expression to CCM1 and CCM2, suggesting a link in its functionality. Currently, no experiments have determined its exact function. The lack of function of these genes in control of a proliferative signaling pathway would result in uncontrolled proliferation and the development of a tumor. In 2018, it was theorized that proliferation of endothelial cells with dysfunctional tight junctions, that are under increased endothelial stress from elevated venous pressure provides the pathophysiological basis for cavernous hemangioma development.
Cavernous hemangioma