Not much is known about how steatosis, which is often present in people with obesity, progresses to nonalcoholic steatohepatitis (NASH). A new paper published in Cell Metabolism implicates the transcription regulator TAZ in this process. The researchers found that levels of TAZ were higher in hepatocytes from humans and mice with NASH than in hepatocytes from normal or steatotic livers. They also silenced TAZ in a mouse model of NASH, which prevented or even reversed hepatic inflammation, hepatocyte death and fibrosis; however, steatosis was not affected. Conversely, when the researchers increased expression of TAZ in hepatocytes, features of NASH developed. Mechanistic studies enabled the team to establish that TAZ promotes fibrosis by inducing expression of Ihh (encoding Indian hedgehog), which increases the expression of profibrotic genes in hepatic stellate cells.