In a recent paper in Gut, Calvaruso et al1 give a succinct summary of the coagulation changes which predispose to fibrosis in chronic liver disease. However, they did not mention the important contribution of the megakaryocyte, in addition to thrombin, to liver fibrosis. This is exemplified by the observation of frequently fatal, liver fibrosis which can occur in acute megakaryoblastic leukaemia (AMKL) and transient myeloproliferative disorder (a precursor of AMKL) in children with Down syndrome.2 These children demonstrate sinusoidal fibrosis and extramedullary haematopoiesis in the liver, raising the possibility that the fibrosis is caused by cytokines elaborated by the liver megakaryocytes.3 Abnormal megakaryocytic progenitor …