As shown by our analyses, MELK inhibition conducted a substantial antitumor role in HCC, which may be partly achieved by CCL2-mediated reprogramming of the crosstalk between HCC cells and the TME to suppress TAM infiltration, interfere with TAM polarization and stimulate CD8 + T-cell recruitment, thereby strengthening antitumor immunity. This evidence concerns the gene CD8A and hepatocellular carcinoma.