The results demonstrated that iLSECs (sorted) showed enriched pathways involved in receptor-mediated endocytosis, coagulation, platelet activation, the Toll-like receptor signaling pathway, the nitric oxide biosynthetic process and receptor-mediated endocytosis of virus by the host cell, whereas the downregulated pathways were associated with LSEC injury, liver inflammation (TGF-β) and dysfunctional LSECs (matrix organization), which are typical features of liver fibrosis. This evidence concerns the gene TGFB1 and Hepatic fibrosis.