Together, these data suggested that CAFs were the main source of STC1 in the HCC TME, and that CAFs and CAF-derived STC1 could promote self-renewal, sorafenib resistance, proliferation, migration, invasion, and G1-S transition of HCC cells and protect HCC cells from sorafenib-induced apoptosis. The gene discussed is STC1; the disease is hepatocellular carcinoma.