Cerebral AVMs are not static congenital formations, they may grow, recur, and even appear de novo after complete resection, embolization, or radiosurgery. The author analyzes modern literature on the molecular mechanisms of AVM growth. The AVM intranidal vessels are exposed to abnormally high blood flows, which leads to the activation of molecular pathways in endothelial cells, causing proliferation and remodeling of AVM vessels. The existence of cerebral AVM is determined by more than 860 genes, the most important among them are the genetic mutations (SNPs) of VEGF, TGF-β, IL-6, MMP, ANG, ENG. The possible causes of AVM relapse after removal or total embolization are described, as well as the mechanisms of stimulation of angiogenesis after partial embolization: hemodynamic changes in AVM, aseptic inflammation in response to embolizate and the local regional hypoxia inside the AVM. In response to this, growth factors are expressed in the endothelium that further stimulate angiogenesis in AVM. Understanding the complex molecular biology of AVMs is critical to identifying and predicting their behavior, developing new treatments that improve the results of endovascular and surgical treatment.