Previous research has indicated the presence of fibromyocytes originating from smooth muscle cells in vascular‐related diseases such as atheroprotective and arteriovenous malformations.[24] Given the higher expression of COL1A1 and COL1A2, lower expression of contractile proteins (TAGLN and MYH11) we annotated this cell population as fibromyocytes (Figure 3A,D). This evidence concerns the gene COL1A2 and arteriovenous hemangioma/malformation.