Association between hepatic steatosis and lipoprotein(a) levels in non-alcoholic patients: A systematic reviewNon-alcoholic fatty liver disease (NAFLD) is the most common cause for chronic liver disease worldwide with a spectrum of presentations ranging from fatty liver to cirrhosis and its complications. Recently, a change in nomenclature of NAFLD was made to metabolic syndrome-associated steatotic liver disease (MASLD) to ratify the role of metabolic syndrome in the disease process. MASLD is associated with disorders of lipid homeostasis [1]. Lipotoxicity in MASLD is driven largely by the increased free fatty acids (FFA) levels in the liver either due to influx or de novo lipogenesis. Lipoprotein(a) (Lp[a]) is a lipid carrying particle known to be associated with increased risk of heart disease in previous epidemiological studies. Cardiovascular disease is the most common cause for mortality in patients with MASLD. Whether Lp(a) has any role in the pathogenesis of NAFLD remains unclear.Masson et al. [2] in their systematic review have reviewed the correlation of Lp(a) with NAFLD. They included 10 observational studies with over 40,000 patients to assess this correlation with exclusion of studies that evaluated patients with cirrhosis. The studies included in this review yielded conflicting results. In patients with NAFLD, while four studies showed lower Lp(a) as compared to controls, one study showed higher levels of Lp(a). Those with non-alcoholic steatohepatitis (NASH) showed no significant difference as compared to controls. In the study with NAFLD and NASH included, patients with NASH had much higher levels of Lp(a) as compared to NAFLD, possibly suggesting a role in driving inflammation. In studies that used the MAFLD terminology, Lp(a) levels were not significantly different from controls. Given the ambiguity in the results, it is unclear is Lp(a) is driving the cardiovascular morbidity and liver-related inflammation in NAFLD. However, this represents an area for future research.