Chemoresistance is the most common cause of chemotherapy failure during breast cancer (BCA) treatment.It is generally known that the mechanisms of chemoresistance in tumors involve multiple genes and multiplesignaling pathways,; if appropriate drugs are used to regulate the mechanisms at the gene level, it should bepossible to effectively reverse chemoresistance in BCA cells. It has been confirmed that chemoresistance in BCAcells could be reversed by ginsenoside Rh2 (G-Rh2). Preliminary studies of our group identified some drugresistancespecific miRNA. Accordingly, we proposed that G-Rh2 could mediate drug-resistance specific miRNAand corresponding target genes through the gene regulatory network; this could cut off the drug-resistanceprocess in tumors and enhance treatment effects. G-Rh2 and breast cancer cells were used in our study. Throughpharmaceutical interventions, we could explore how G-Rh2 could inhibit chemotherapy resistance in BCA,and analyze its impact on related miRNA and target genes. Finally, we will reveal the anti-resistance molecularmechanisms of G-Rh2 from a different angle in miRNA-mediated chemoresistance signals among cells.