The involvement of inflammation in the development of post-MI HF has already been established; according to an experimental study in mice, angiotensin II exerts myocardial damage post-MI through the attachment of the pro-inflammatory Nox2+ myelomonocytic cells, macrophages, and monocytes at the vessel wall along with stimulation of oxidative stress and the ED [131]. Here, CYBB is linked to myocardial infarction.