## 1 Introduction  
The term steatosis refers to the accumulation of fat within cells. When this process occurs in liver cells, it is termed \"liver steatosis\" or \"fatty liver\". Non-alcoholic fatty liver disease (NAFLD) encompasses a wide spectrum of chronic liver diseases characterized by the presence of hepatic steatosis, which can be confirmed either through histological evaluation via liver biopsy (the gold standard) [1] or through imaging techniques that document at least 5% steatosis in the hepatic parenchyma [2]. NAFLD is distinguished from secondary causes of fat accumulation [3], such as excessive alcohol consumption [4], hereditary disorders (e.g., [PERSON]'s disease), or the use of drugs known to induce steatosis (e.g., amiodarone, steroids, tamoxifenfen) [5].  
The most significant risk factors for NAFLD include metabolic syndrome, obesity, insulin resistance/type 2 diabetes mellitus, and dyslipidemia [1]. Recently, the term NAFLD has been replaced by metabolic-dysfunction-associated steatotic liver disease (MASLD) to better reflect the association of hepatic steatosis with at least one cardiometabolic risk factor (e.g., obesity, hypertension) [6].  
NAFLD can progress to non-alcoholic steatohepatitis (NASH), a condition characterized by both steatosis and inflammation, which can lead to fibrosis and, ultimately, cirrhosis. Under the new nomenclature, MASLD may progress to metabolic-dysfunction-associated steatohepatitis (MASH).  
The natural history of NAFLD is not fully understood [2]. The prevailing theory is the \"multiple hit\" hypothesis, which suggests that genetically predisposed individuals (with genetic variations such as patatin-like phospholipase domain-containing protein 3--PNPLA3, transmembrane 6 superfamily 2--TM6 SF2, or membrane-bound O-acyltransferase domain-containing protein 7--MBOAT7 [7]) are affected by environmental factors (e.g., lifestyle, gut microbiome, dietary habits) that lead to lipid accumulation, increased hepatic de novo lipogenesis, and impaired inhibition of adipose tissue lipolysis. These processes result in hepatic fat accumulation and the creation of a lipotoxic environment, triggering mitochondrial dysfunction, reactive oxygen species (ROS) production, and endoplasmic reticulum stress.  
Cellular damage initiates immune cell infiltration, fibrogenesis, and hepatic progenitor cell activation. Additionally, as MASLD [8] is closely linked to metabolic disorders, it is often accompanied by adipose tissue dysfunction and increased secretion of adipokines and proinflammatory cytokines. These processes exacerbate oxidative stress and cause DNA damage in liver cells, promoting fibrosis and cirrhosis [9,10]. Chronic hepatic inflammation may be the driving force behind the progression of MASLD to hepatocellular carcinoma (HCC). However, it is important to emphasize that our understanding of the pathogenesis and progression from MASLD to HCC remains limited. Nevertheless, given that increased hepatic inflammation has been independently associated with a higher risk of HCC--even in individuals with non-cirrhotic MASLD--it is reasonable to attribute a role to MASLD-related inflammation in tumor development. This underscores the critical involvement of inflammatory pathways in the pathogenesis of HCC in patients with MASLD [11]. As previously mentioned, further research is needed to explore additional mechanisms underlying the progression from MASLD to HCC.