This finding is interesting in light of recent evidence demonstrating that oxidative/ER stress are key factors, which trigger NAFLD progression from simple steatosis toward NASH, as well as further aggravation to HCC.1 However, we surmise that, at this juncture, we cannot delineate whether the alterations in oxidative and ER stress in TAOK1-deficient hepatocytes were secondary to the reduction in cellular lipid accumulation or were mediated by a different pathway controlled by TAOK1. This evidence concerns the gene TAOK1 and metabolic dysfunction-associated steatotic liver disease.