These findings underscore four core principles of chronotherapeutic MRIS management: Dawn BMAL1 activation upregulates hepatic CPT1A, driving peak FAO at sunrise, a rhythm exploited by administering CPT1A inhibitors at dawn to maximally suppress pathological lipid flux; dusk NAMPT expression peaks optimize NAD+ precursor efficacy; nighttime PER2-mediated NOX4 suppression enables antioxidant repair; and feeding cycle-synced SCFA production reduces morning endotoxemia [42, 190, 264]. The gene discussed is BMAL1; the disease is serum lipopolysaccharide activity.