In summary, in the current investigation on the function of TRAF6 in TNBC chemoresistance and glucose metabolism, we identified a brand‐new cancer‐driving role of the TRAF6/PKM2/STAT3 axis based on the evidence that TRAF6 interacted with PKM2 to enhance glycolysis and then promote TNBC chemoresistance by activating STAT3 at the level of phosphorylation, and that TRAF6 boosted PKM2‐mediated drug resistance of TNBC in the xenograft models and clinical tumor tissues. This evidence concerns the gene STAT3 and neoplasm.