The results showed that miR-144 or miR-451a overexpression in Hepa1–6 cells generated media that promoted M1 polarization of BMDMs, as revealed by an increased production of M1-type cytokines and nitric oxide (NO) when untreated or subjected to LPS/IFN-γ stimulation for M1 polarization (Fig. S10A-C); expression of miR-144 or miR-451a in HCC cells also impaired the BMDM response to stimuli for M2 polarization since both the secretion of M2-type cytokines and the expression of CD206 and arginase 1 were repressed by these miRNAs (Fig. S10A, B, D). This evidence concerns the gene ARG1 and hepatocellular carcinoma.