Recent research has highlighted the molecular underpinnings of AVMs, including germline mutations in ENG (endoglin), ACVRL1 (activin receptor-like kinase 1), and SMAD4 (Mothers against decapentaplegic homolog 4) in HHT, as well as somatic mutations in KRAS (Kirsten rat sarcoma virus), MAP2K1 (Mitogen-activated protein kinase kinase 1), and PIK3CA (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha) in sporadic lesions [4,18,19,24,25,26,27,28,29,30]. This evidence concerns the gene PIK3CA and hereditary hemorrhagic telangiectasia.