As for the molecular mechanisms by which HBx regulates CD68+ TAMs in HCC, our previous findings revealed that HBx could promote stromal cell-derived factor-1 (SDF-1) secretion and exert downstream effects by binding to its ligand C-X-C chemokine receptor 4 (CXCR4) [11], while interaction with SDF-1 and CXCR4 was shown to drive recruitment and M2-type polarization of TAMs in HCC, thus inducing an immunosuppressive microenvironment and accelerating tumor progression [38]. The gene discussed is CXCR4; the disease is neoplasm.