AMPK mitigates myocardial remodeling and fibrosis by suppressing excessive autophagy and correcting lipid metabolism disorders in cardiomyopathy, while STAT3, which binds to promoters of ferroptosis-related genes such as SLC7A11 and GPX4, can promote ferroptosis and exacerbate pathology in non-tumor contexts [60]. The gene discussed is SLC7A11; the disease is neoplasm.