Vascular malformations result from anomalies in the angiogenesis process; they are subdivided into capillary, lymphatic, venous, arteriovenous, and mixed malformations, according to the type of affected vessels. Vascular anomalies occur typically by sporadic somatic gene mutations, while familial forms are relatively rare. Mostly, mutations are detected in genes that play important roles in pathways involved in angiogenesis, vascular cell growth, apoptosis, and proliferation. The major pathways which are linked to the development of vascular malformations are the phosphoinositide 3-kinase (PI3K)-protein kinase B (AKT)-mammalian target of rapamycin (mTOR) and the mitogen-activated protein kinase cascade (MAPK). Deeper insights into these genetic anomalies have paved the way for exploring targeted therapeutic interventions and for repurposing anti-cancer drugs. These treatments aim to specifically target and disrupt the identified signaling pathways, effectively “normalizing” their excessive activation.