H19 and metabolic dysfunction-associated steatotic liver disease: While the basal expression level of lncRNA H19 in the liver remains low under normal physiological conditions, it exhibits a propensity for up-regulation during pathological states.[10] Previous animal studies[11,12] have demonstrated that lncRNA H19 expression is upregulated during the development of oleic acid-induced steatosis and high-fat diet-induced NAFLD mouse models, leading to lipid accumulation in hepatocytes.