Myeloid‐Mas Signaling Modulates Pathogenic Crosstalk among MYC+CD63+ Endothelial Cells, MMP12+ Macrophages, and Monocytes in Acetaminophen‐Induced Liver Injury

macrophages, and monocytes, which is maintained by enhanced glycolysis and the NF-κB/TNF-α signaling pathway due to myeloid-Mas deficiency. Importantly, the pathogenic microenvironment is delineated in samples obtained from patients with ALF, demonstrating its clinical relevance. In summary, these findings greatly enhance the understanding of the microenvironment in advanced AILI and offer potential avenues for patient stratification and identification of novel therapeutic targets.