In summary, the observations communicated here provide valuable evidence regarding a hepatocardiorenal syndrome [15] induced by chronic administration of a diet with a high-lipid content, in which abnormal upregulation of the Ang-(3–4)-sensitive Ang II→AT1R axis of RAAS culminates with connected cardiac and renal fibrosis, liver steatosis, arterial hypertension, and augmented renal Na+ reabsorption [1] as the prominent pathological disturbances. The gene discussed is ANG; the disease is Hypertension.