These effectors have been extensively researched and their crucial roles in TAM recruitment and polarization have been well‐established.[32, 33] We have detected CCL2 and CSF1 expression in both activated HSCs and hepatoma cells, which may explain why only a double knockout of ASH1L in both cell types, rather than a single knockout in either cell type, can alleviate the development of fibrosis‐associated HCC. The gene discussed is CCL2; the disease is hepatocellular carcinoma.