Groundbreaking research, initially published in *Nature Metabolism* and reported by the European Medical Journal, has identified the liver-specific receptor GPR110 as a crucial determinant in the sex-specific progression of metabolic dysfunction-associated steatohepatitis (MASH). MASH, an advanced stage of metabolic dysfunction-associated steatotic liver disease (MASLD), poses a significant global health challenge, often progressing silently to severe conditions like cirrhosis with limited treatment options. The study elucidated that GPR110 plays a pivotal role in mediating these sex-related disparities, primarily through its interaction with estrogen receptor alpha (ERα) signaling pathways in the liver. Researchers demonstrated that the deletion of hepatocyte-specific Gpr110 remarkably protected female mice from developing MASH, including liver inflammation and fibrosis, a protective effect notably absent in male mice. This finding underscores GPR110's sex-specific function in disease progression. Further analysis revealed that the absence of GPR110 led to increased estrogen receptor activity in female liver cells, correlating with reduced liver injury. Translational implications are significant, as the research also identified a genetic variant in the human GPR110 gene (rs937057 T > C) linked to a higher prevalence of MASLD in women. These discoveries suggest that targeting GPR110 could offer a novel, sex-specific therapeutic strategy for MASH, potentially restoring estrogen receptor alpha activity in women and mitigating liver inflammation and fibrosis. This insight represents a major step towards personalized medicine in addressing this increasingly prevalent liver disease.