Suppression of FLCN in the liver by Bridget S. Gosis et al. has been shown to protect mice against NAFLD and partially reverse these processes, indicating that FLCN could be a therapeutic target for NAFLD.1 Hepatocyte-specific FLCN deletion in mice preferentially inhibits mTORC1-mediated phosphorylation of TFE3 and promotes its entrance into the nucleus, but has a modest effect on the canonical substrates S6K and 4E-BP1. Here, TFE3 is linked to metabolic dysfunction-associated steatotic liver disease.