The model is consistent with observation of increased IL-1β in patients with NASH and fibrosis (133, 134); increased number of IL-1β positive liver cells in mice fed a high fat and cholesterol diet (135); that the lack of IL-1β inhibits the transformation of steatosis to steatohepatitis (136); and that deficiency of hepatic- rather than bone marrow-derived IL-1β protected mice against development of steatohepatitis and liver fibrosis on an atherogenic diet (136). This evidence concerns the gene IL1B and fibrosis.