The capacity of AnxA1 to interfere with the CCL2/CCR2 axis might be particularly relevant in relation to the evolution of steatohepatitis, because CCR2 deficiency and CCR2 antagonism ameliorate liver injury and fibrosis in experimental NASH.30,31 Possibly unrelated to the IL-10 effect discussed above, AnxA1-mediated CCR2 down-regulation provides further mechanistic support to the “protective” role played by this mediator. The gene discussed is CCL2; the disease is metabolic dysfunction-associated steatohepatitis.