This study has inherent limitations: (1) mechanistic validation remains based on cellular models, necessitating macrophage-specific MEK1-knockdown models for in vivo confirmation; (2) the downstream effectors of CHEK2 in mitophagy regulation require elucidation; and (3) murine data need validation in clinical samples (e.g., MEK1 activity in CD68+ macrophages from osteomyelitis patients). The gene discussed is MAP2K1; the disease is osteomyelitis.