In a model of doxorubicin‐induced cardiomyopathy and fibrosis, activating the AMPK/ULK1/FUNDC1 pathway reduces ROS levels, improves mitochondrial membrane potential, and increases mitophagy, thereby ameliorating cardiomyopathy (Zhao et al. 2024). Here, ULK1 is linked to cardiomyopathy.