Hepatocytes, cholangiocytes, putative hepatobiliary progenitor cells and fibroblasts express functional interleukin-4 and interleukin-13 receptors, and studies conducted on transgenic mice with interleukin-13 signaling genetically disrupted in hepatocytes, cholangiocytes or fibroblasts revealed key roles for interleukin-13 in fibrosis, steatosis, cholestasis and ductular reaction [36]. The gene discussed is IL13; the disease is steatosis.