Since Ang II promotes cardiac hypertrophy and fibrosis not only directly but also through upregulation of the transcription and synthesis of TGF-β1 and MMPs, which also contribute to such cardiac remodeling [19,20], in this Ang II infusion model, chymase inhibitors might attenuate cardiac remodeling—despite elevated systemic Ang II levels—through suppression of TGF-β1, MMP-2, and MMP-9 activation, rather than by reducing Ang II production alone. The gene discussed is AGT; the disease is cardiac hypertrophy.