Heterozygous mutations in the MYH11 gene affecting the C-terminal coiled-coil region of the smooth muscle myosin heavy chain, a contractile protein of smooth muscle cells (SMC), have been described to cause thoracic aortic aneurysm or aortic dissection (TAAD) and patent ductus arteriosus (PDA).1 Herein we expand the phenotype associated with MYH11 mutations to include moyamoya-like cerebrovascular disease. This evidence concerns the gene MYH11 and Patent ductus arteriosus.