Fibrosis stage represents the strongest predictor of both liver-related and all-cause mortality in metabolic dysfunction-associated steatotic liver disease (MASLD), while GLP-1 receptor agonists and dual incretin therapies demonstrate substantial hepatic benefits beyond glucose control. The disease affects over 1 billion people worldwide as obesity's primary liver manifestation, progressing through cascading metabolic dysfunction involving adipose tissue breakdown, insulin resistance, and gut-liver axis disruption. This comprehensive review validates a critical shift in therapeutic thinking. Rather than targeting liver fat accumulation directly, successful interventions now focus on upstream metabolic drivers—particularly incretin pathways that regulate both glucose metabolism and hepatic lipid processing. The emergence of distinct MASLD phenotypes, including lean variants, challenges traditional obesity-centric models and supports personalized treatment approaches. However, the field still grapples with substantial limitations: lifestyle interventions show poor long-term adherence, and most pharmacologic data comes from relatively short-term studies. The mortality prediction power of fibrosis staging represents perhaps the most clinically actionable finding, enabling earlier risk stratification before irreversible liver damage occurs. This paradigm shift toward metabolic-first treatment strategies could transform outcomes for the growing population facing this silent epidemic.