Knocking out Slc7a11 in mice exacerbates cardiomyocyte hypertrophy, increases myocardial PTGS2, MDA, and ROS levels, and worsens Ang II-mediated cardiac hypertrophy and dysfunction, all of which can be prevented by overexpressing SLC7A11.318 Interestingly, treatment with Fer-1 in Slc7a11 knockout mice inhibits cardiomyocyte hypertrophy.318 These findings suggest that SLC7A11 may alleviate Ang II-induced myocardial hypertrophy by inhibiting ferroptosis and upregulating SLC7A11 could be a novel therapeutic approach for treating cardiac hypertrophic diseases. The gene discussed is AGT; the disease is cardiac hypertrophy.