Furthermore, in addition to a decrease in phosphorylation of the MLC, ID reduced the expression of F‐actin, integrinβ1, and Cdc42, while increasing the expression of Rac1 both in vivo and in vitro, which are important molecular in cytoskeleton and function, and promote the proliferation and migration of VSMCs, thereby indicating that ID may contribute to the formation of AD by changing the morphology and function of VSMCs. This evidence concerns the gene RAC1 and Alzheimer disease.