MOTS-c expression declines post-irradiation, whereas exogenous MOTS-c attenuates mitochondrial ROS production, preserves mitochondrial homeostasis, and mitigates alveolar epithelial cell apoptosis via activation of the Nrf2/ARE pathway, thereby alleviating radiation pneumonitis (Zhang et al., 2024b; 2024a). This evidence concerns the gene MT-RNR1 and radiation pneumonitis.