For now, working hypotheses might be developed along two lines respectively involving disturbed lipid handling [5, 17–19], a key mechanism in atherosclerosis, or the involvement of MEOX2 in the angiogenic responses to stressors [20–24] or in the migration or proliferation of endothelial and vascular smooth muscle cells [25, 26]. The gene discussed is MEOX2; the disease is atherosclerosis.