Metabolic dysfunction associated steatotic liver disease (MASLD), previously known as non alcoholic fatty liver disease (NAFLD), is now recognized as the most common cause of chronic liver disease globally. The disease spectrum ranges from simple steatosis to steatohepatitis and advanced fibrosis. Fibrosis stage is the most significant determinant of long term outcomes including cirrhosis and hepatocellular carcinoma. In India, the prevalence of MASLD is estimated at 15 to 32 percent in urban populations, reflecting rising rates of metabolic syndrome and dyslipidemia. Notably, a substantial subset of patients are non diabetic but still demonstrate metabolic risk factors and progressive fibrosis. To date, lifestyle modification, primarily weight loss through diet and exercise, remains the cornerstone of MASLD management. However, achieving and sustaining 7 to 10 percent weight reduction, which is required to induce fibrosis regression, is notoriously difficult in real world settings. International guidelines consistently acknowledge the absence of a universally effective, approved pharmacological therapy for MASLD. Several investigational agents have shown promise in early trials but have failed to demonstrate histologic benefit or safety in phase 3 studies, underscoring the complexity of MASLD pathogenesis and drug development. This therapeutic vacuum has created a pressing need to identify agents that are safe, accessible, and effective in modifying both metabolic dysfunction and hepatic fibrosis. Saroglitazar, a dual PPAR agonist developed in India, is an established therapy for diabetic dyslipidemia . It enhances fatty acid oxidation and improves insulin sensitivity, leading to reductions in hepatic steatosis and inflammation . Clinical trials and real world studies have demonstrated reductions in liver stiffness, aminotransferases, and hepatic fat content following saroglitazar therapy in MASLD. However, limited data exist specifically for non diabetic MASLD patients with advanced fibrosis. This represents a crucial gap in the literature. Non diabetic MASLD patients are frequently overlooked in clinical pathways due to the misconception that metabolic risk and fibrosis progression are tightly linked to diabetes. Yet, Indian studies demonstrate that non diabetic individuals may harbor significant hepatic injury driven predominantly by dyslipidemia, visceral adiposity, and genetic predisposition. In such patients, early therapeutic intervention could potentially halt disease progression before cirrhosis develops. Furthermore, as saroglitazar is already approved and widely used for diabetic dyslipidemia, evaluating its role in this specific MASLD subgroup is both clinically relevant and immediately translatable. This study aims to evaluate the efficacy and safety of saroglitazar in non diabetic MASLD patients with advanced fibrosis over 52 weeks, using changes in FibroScan derived liver stiffness as the primary endpoint.