Furthermore, it was also shown that mice can be protected from arterial hypertension when LysM-positive cells are depleted before the AngII infusion is begun and that BP can be restored by adoptive transfer of Nox2-competent monocytes into these mice.16 Taken together, these data indicate complex roles during AngII-induced hypertension for Nox2 in multiple cell types, some that involve altered NO bioavailability and others that may involve Nox2-dependent redox signaling events. The gene discussed is AGT; the disease is Hypertension.