Is liver steatosis a disease or the emperor’s new clothes?

The redefinition of steatotic liver disease, including metabolic dysfunction-associated steatotic liver disease (MASLD) and steatohepatitis (MASH), has sharpened the distinction between benign hepatic fat accumulation and true liver pathology. MASLD has a global prevalence of 25-30%, but this should not be regarded as the prevalence of individuals with liver disease requiring diagnosis and treatment, as only a minority will progress to advanced disease with liver-related morbidity or mortality. Steatosis alone is often a phenotype or risk marker for liver disease or cardiometabolic disease - not a disease per se in the conventional sense. Clinically relevant liver disease arises when steatosis progresses to steatohepatitis and fibrosis -conditions identifiable by emerging non-invasive tests or histology. MASH has a substantial global prevalence of around 5%. The risk of adverse liver outcomes in MASLD/MASH is primarily determined by the stage of liver fibrosis (e.g. liver stiffness >10 kPa by elastography), severity of metabolic dysfunction (e.g. type 2 diabetes) and other risk factors (e.g. alcohol, genetics, age and sex). From a therapeutic perspective, this distinction underscores that isolated steatosis warrants primarily cardiometabolic management, whereas both established MASH and MASLD with fibrosis require liver-targeted interventions. Recognising the difference between steatosis (not a standalone liver disease) and MASH/fibrosis (true driver of liver-related risk) enables more precise risk communication, guides targeted surveillance and treatment, and helps to avoid unnecessary alarm and inefficient use of resources in already strained healthcare systems. This paradigm shift supports credible, evidence-based public health strategies focused on metabolic health and fibrosis prevention.