In our study, we discovered that TRAF6 was expressed more significantly in the case of triple‐negative breast cancer (TNBC) than in other of breast cancers, promoting chemoresistance to paclitaxel; that inhibited TRAF6 expression in the chemoresistant TNBC (TNBC‐CR) cells enhanced the sensitivity by decreasing glucose uptake and lactate production; that TRAF6 regulated glycolysis and facilitated chemoresistance via binding directly to PKM2; and that overexpressing PKM2 in the TNBC‐CR cells with TRAF6 knocked down regained significantly TRAF6‐dependent drug resistance and glycolysis. The gene discussed is PKM; the disease is breast carcinoma.