Kamiya et al. (2021) found that C57BL/6J mice treated with Ang II showed a significant increase in LVEDP and end-diastolic pressure-volume at the 4th week. Significant fibrosis and cardiac hypertrophy were also observed in the Ang II group, with no significant difference in LVEF and E/A. They also found that Ang II-mediated cardiac fibrosis was dependent on a cardiac cytokine, transforming growth factor (TGF)-β1. However, ANG II has also been used to establish animal models for HFrEF (Pan G et al., 2018). This evidence concerns the gene AGT and cardiac hypertrophy.