Thus far, AnxA1 has been implicated in reducing granulocyte-tissue infiltration by blocking neutrophil-endothelial interactions and accelerating neutrophil apoptosis.6,7 Neutrophil infiltration is not relevant in the pathogenesis of NASH, whereas macrophages and lymphocytes are the predominant inflammatory cells.29 Thus, our data point to the possibility that, during chronic inflammation, AnxA1 might also control the recruitment of monocytes. The gene discussed is ANXA1; the disease is metabolic dysfunction-associated steatohepatitis.