Metabolic dysfunction-associated steatotic liver disease affects nearly one billion people globally, yet therapeutic options remain limited despite the condition's role as a precursor to cirrhosis and liver cancer. This research gap has made the liver's fatty acid synthesis machinery an increasingly attractive therapeutic target. Chinese researchers have identified a promising experimental compound, 84-B10, that appears to combat liver fat accumulation through a novel mechanism involving fatty acid synthase (FASN) protein degradation. Unlike existing approaches that typically inhibit FASN enzyme activity, 84-B10 promotes the breakdown of the FASN protein itself, potentially offering more sustained therapeutic effects. The compound demonstrated efficacy in laboratory models of MASLD, suggesting it could address the underlying metabolic dysfunction rather than merely managing symptoms. This protein degradation approach represents a sophisticated strategy that could overcome resistance mechanisms often seen with traditional enzyme inhibitors. The targeting of FASN is scientifically sound given the enzyme's central role in converting excess carbohydrates into stored fat within liver cells. However, several critical questions remain unanswered. The research appears to be in early preclinical stages, and the compound's safety profile, optimal dosing, and long-term effects require extensive investigation. Additionally, the transition from laboratory models to human physiology often reveals unexpected challenges, particularly for liver-targeted therapeutics. While 84-B10's unique mechanism offers theoretical advantages over existing FASN inhibitors, the liver disease field has witnessed numerous promising compounds fail in later-stage clinical testing due to toxicity or insufficient efficacy.