However, we found no evidence to support a meaningful role for IL6 or IL11 trans-signaling in a biologically relevant context either in vitro or in vivo, using both gain- and loss-of-function approaches. Notably, sgp130, a therapeutic agent that inhibits IL6 trans-signaling, had no effect on lipotoxicity, NAFLD or NASH.  Thus, we suggest that IL6 family member trans-signaling has no role in hepatocytes or NASH, which is in agreement with studies outside the liver20,21. Here, IL6 is linked to metabolic dysfunction-associated steatotic liver disease.