Importantly, genetic knock-out of JAM-B or treatment with soluble recombinant JAM-C fragment inhibited fibrogenesis in the AIH mouse model without affecting hepatic leukocyte infiltration [164], suggesting that blockade of sinusoidal EC/pericyte or pericyte/pericyte interactions might be a strategy to block fibrosis independent of the cause of chronic liver damage. The gene discussed is JAM3; the disease is autoimmune hepatitis.