First, although AAV or adenovirus‐mediated overexpression or knockdown has been widely used in the field of liver research, future work using liver‐specific knockout mice will further validate the role of long‐term NR2F6 depletion in the development of NAFLD and NASH, especially under the conditions of different metabolic status. Here, NR2F6 is linked to metabolic dysfunction-associated steatotic liver disease.