[29] The deposition of the extracellular matrix can lead to a decrease in the activity of matrix metalloproteinases (MMPs), which is conducive to the formation of fibrotic scars.[30] In most liver disease studies, it has been found that the main source of α-SMA-expressing fibroblasts is HSCs.[31] Thus, we cocultured HSCs with HCC cells; this coculture system activated the HSCs, which played a role similar to that of CAFs. The gene discussed is ACTA1; the disease is liver disorder.