Although there has been much work on the actions of JNK and p38 MAPK in the development of NAFL8,9,14–17 the role of hepatic MAPKs in promoting the essential pro-inflammatory “hit” required to drive fibrosis in the transition from NAFL to NASH has not been formally demonstrated. This evidence concerns the gene MAPK8 and metabolic dysfunction-associated steatohepatitis.