Whereas adoptive cell transfer of wildtype monocytes to the ablated mice restored all adverse effects of Ang II, the transfer of monocytes from mice lacking the Ang II type 1 receptor (AT1R) or the phagocytic NADPH oxidase (NOX2) failed to restore hypertension and other complications, supporting a central role of Ang II type 1 receptor (AT1R)-NOX2 signaling for Ang II-conferred adverse effects [6]. The gene discussed is AGT; the disease is Hypertension.