Our results showed that the PI3K/Akt pathways were inhibited after the downregulation of MyD88 or the overexpression of miR-149-5p, compared to that in the control cells; in addition, our results showed that the expression of Bax was increased while the expression of Bcl-2 was decreased in 231/PTX cells compared to those in the control cells, which suggests that MyD88 mediated PTX resistance through the PI3K/Akt pathway in breast cancer cells. The gene discussed is AKT1; the disease is breast carcinoma.