Similarly, the whole-proteome Mendelian-randomization study by Li et al identified several ECM regulators (including CTSD) as causal drivers of NAFLD, underscoring the therapeutic promise of ECM-targeted interventions.[25] Collectively, these data advocate co-targeting pro-fibrotic effectors (LIGHT, CTSD) alongside anti-fibrotic counterparts (BMP-7, GNMT) rather than relying on single-agent blockade. This evidence concerns the gene CTSD and metabolic dysfunction-associated steatotic liver disease.