Ko et al. [86] revealed that a lack of M-CSF in mice caused milder vascular remodeling, endothelial dysfunction, and oxidative stress stimulated by deoxycorticosterone acetate (DOCA)-salt than +/+ and osteopetrosis (Op)/+ mice, indicating that inflammation might play a key role in DOCA-salt caused hypertension [86]; see Table 22. The gene discussed is CSF1; the disease is endothelial dysfunction.