Various factors originating from dysfunctional endothelial cells induce FOXM1 expression in smooth muscle cells (SMCs) and trigger FOXM1-dependent SMC proliferation, which contributes to atherosclerosis, aortic aneurysm, pulmonary vascular remodeling and pulmonary hypertension [31,32]. This evidence concerns the gene FOXM1 and pulmonary arterial hypertension.