Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) in patients with no or very little alcohol consumption is characterised by hepatic histological changes similar to those associated with alcohol-induced liver injury. A range of histological changes can be seen. Some patients have fat accumulation in hepatocytes without significant inflammation or fibrosis (simple hepatic steatosis or NAFLD), but others have hepatic steatosis with prominent necro-inflammatory changes with or without associated fibrosis (this is NASH). Although NAFLD and NASH are common conditions, no effective medical treatment is available to correct the abnormal liver enzymes and adverse outcomes associated with them. This systematic review identified two randomised clinical trials with very small numbers of participants. One of the trials was a pilot trial and compared simvastatin with placebo, and the other trial assessed atorvastatin versus fenofibrate versus a combination of the two. The small pilot trial (n = 16 patients) assessing simvastatin versus placebo in NASH patients did not show significant effects on liver enzyme activities or liver histology. No adverse events were reported. The other trial compared atorvastatin versus fenofibrate versus a group receiving both interventions in 186 patients with NAFLD. There were no statistically significant differences between any of the three intervention groups regarding the 54 week mean activities of aspartate aminotransferase, alanine aminotransferase, gamma-glutamyl transpeptidase, or alkaline phosphatases (liver enzymes) in the blood. The triglyceride levels seemed higher in the fenofibrate group compared with the atorvastatin group. Liver histology was not assessed in this trial. The presence of biochemical and ultrasonographic evidence of NAFLD seemed higher in the fenofibrate group compared with the other two intervention groups. Three patients discontinued treatment due to myalgia and elevated serum creatine kinase activity, one from the atorvastatin group and two from the combination group. Another patient from the atorvastatin group discontinued treatment due to raised alanine aminotransferase activity, over three times the upper normal limit. Both trials were at high risk of bias (that is, overestimation of benefits and underestimation of harms). Furthermore, the groups were small raising the risks of random errors (that is, play of chance). Accordingly, we did not find evidence to support or refute the use of statins for patients with NAFLD or NASH. Further unbiased trials with larger numbers of patients looking explicitly at patient-related outcomes of interest (for example, quality of life, development of cirrhosis, and mortality) are needed to assess the effects of statins on NAFLD or NASH.