Discussion CM-AVM is an autosomal dominant disorder with high penetrance and de novo onset.1 The incidence of CM-AVM syndrome is unknown. In the first large study reported in the literature, 45 out of 140 individuals came from a French-speaking Belgian population of 4 million people, with an estimated prevalence of 1 in 100,000 Caucasians (Revencu, 2008).3 In our area, we found a similar prevalence, that is, seven cases in a population of 820,000 people (0.85/100,000). CM-AVM is a clinically and genetically heterogeneous syndrome,1-14 and its clinical diagnosis is based on the identification of CM-small and multifocal features. Since large CMs up to 15 cm can occur and the reported number of CMs in individual cases can range from 1 to 60, evidence of RASA1 mutation or a family history of CM or AVM allows the diagnosis of equivocal cases. Probable or definitive diagnostic categories have been proposed for this entity (Orme 2013).4 AVMs appear in one-third of individuals with CM-AVMs and can occur on the skin, muscles, bones, spine, and brain; however, the liver and lungs are not involved.6 In a recent literature review, symptomatic spinal or intracranial AVMs occurred in more than 7% of patients with this syndrome and usually manifested symptoms within the first 7 years of life ( Orme 2013).4 Furthermore, in a retrospective study, 43% of children who presented with cerebral hemorrhage secondary to arteriovenous malformation exhibited the CM-AVM phenotype (Chee 2010).15 This potentially serious morbidity has raised concerns about the use of brain and spinal MRI as a screening tool in all patients. Management is still controversial because many affected individuals with or without AVM are asymptomatic and have not been defined… halfway through the article… involved in hair follicle proliferation and cell cycle. However, the limited number of patients examined limits our study. Therefore, it is necessary to evaluate hair reduction on CMs in larger series to determine whether this finding may be useful for differentiating between lesions associated with CM-AVM syndrome and other CMs, such as classic PWS. In conclusion, our study confirms that small anemic white halos with red dotted spots on the upper extremities or small clustered telangiectasias on the neck or upper trunk are frequent findings in CM-AVM syndrome. Furthermore, the alopecia observed on CMs suggests that RASA1 gene mutations may be involved in hair follicle proliferation and cell cycle. Further studies are needed to confirm this association and it would be interesting to study new therapies for hair disorders such as alopecia and hirsutism