dysregulated genes were found in women with MASLD compared with men. Interestingly, most of the pathways identified were common in both sexes, except for those involved in bile acid, bile salt metabolism, and O-linked glycosylation, which were only found in men. hepatic proportions of scar-associated mesenchymal, plasma, arterial, and lymphatic endothelial cells were found to be predictive of higher all-cause mortality and decompensation events, whereas higher proportions of homeostatic liver-resident cell types, including vascular smooth muscle cells and liver sinusoidal endothelial cells, were protective. scriptional risk score for hepatic decompensation, achieving areas under the receiver operating characteristic curves of 86.24%, 83.26%, and 80.97% for predicting 1, 3, and 5-year risk of decompensation events, respectively. Finally, they investigated transcription factor-regulated gene networks, termed regulons, that were associated with disease progression and determined that thyroid hormone receptor beta (THRB) regulon activity was a critical suppressor of MASLD progression. Using THRB regulon activity cutoffs, the team was able to differentiate individuals at high risk of rapid progression to decompensation events at early, stage 0-1, fibrosis. The main limitation of this study centers around the homogeneity of the study population, challenging the generalizability of the findings. At present, the costs and complexity of the analysis limit translation to the clinic.