CHs are histologically classified into cavernous, capillary, and arteriovenous malformation subtypes, among which the cavernous type constitutes approximately 58.5% of cases (1, 2) The pathogenesis of CH remains incompletely elucidated, though studies have identified dysregulation of the vascular endothelial growth factor (VEGF) and VEGF receptor (VEGFR) signaling pathway in vascular tumors and malformations (3), suggesting a potential association with vascular endothelial injury. This evidence concerns the gene VEGFA and cyclic hematopoiesis.