Indeed, our data in resident failing hearts who were treated with RAS-inhibition, evidenced higher myocardial GlycACE2, NFAT and cardiac fibrosis along with reduced levels of Ang 1–7, Ang 1–9, and MasR supporting an impaired cardioprotective effect of RAS-inhibition in diabetic patients with severe HF compared to nondiabetic patients. This evidence concerns the gene ANGPT1 and hydrops fetalis.