The article discusses the molecular mediators of hepatic steatosis and liver injury, focusing on nonalcoholic fatty liver disease (NAFLD) and its progression to steatohepatitis (NASH). NAFLD is a common condition associated with obesity and insulin resistance, characterized by the accumulation of triglycerides in the liver. The progression from NAFLD to NASH involves a series of molecular and physiological changes, including increased lipogenesis, oxidative stress, and mitochondrial dysfunction. Key transcription factors such as SREBP-1c, ChREBP, and PPAR-γ play crucial roles in regulating lipid metabolism and contributing to hepatic steatosis. AMP-activated protein kinase (AMPK) is another important regulator that can reduce lipogenesis and improve liver function. The article highlights the need for further research to understand the exact mechanisms by which hepatic steatosis progresses to NASH and to develop targeted interventions for preventing this progression.The article discusses the molecular mediators of hepatic steatosis and liver injury, focusing on nonalcoholic fatty liver disease (NAFLD) and its progression to steatohepatitis (NASH). NAFLD is a common condition associated with obesity and insulin resistance, characterized by the accumulation of triglycerides in the liver. The progression from NAFLD to NASH involves a series of molecular and physiological changes, including increased lipogenesis, oxidative stress, and mitochondrial dysfunction. Key transcription factors such as SREBP-1c, ChREBP, and PPAR-γ play crucial roles in regulating lipid metabolism and contributing to hepatic steatosis. AMP-activated protein kinase (AMPK) is another important regulator that can reduce lipogenesis and improve liver function. The article highlights the need for further research to understand the exact mechanisms by which hepatic steatosis progresses to NASH and to develop targeted interventions for preventing this progression.