As Schmit et al. pointed out, it could also be stipulated that the hyperangiogenic microenvironment predominant in MMD, in conjunction with a local proangiogenic stimulus (for instance VEGF or fibroblastic growth factor—FGF) as a consequence of cerebral infarction, would have been sufficient for an AVM to develop on that precise spot [98]. The gene discussed is VEGFA; the disease is multiminicore myopathy.