While it remains feasible that high sICAM-1 levels in SVD patients could stem from beyond the brain endothelium, ICAM-1 is a heterogeneous molecule and can influence endothelial function through dysfunctional crosstalk involving other cells in the brain that can also derive it, including monocytes, macrophages, smooth muscle cells and pericytes [53]. This evidence concerns the gene ICAM1 and snowflake vitreoretinal degeneration.