Since autophagy often acts as a pro‐survival response to chemotherapeutic treatment in cancer cells, and suppression of autophagy during chemotherapy has been proposed as a novel therapeutic strategy.[34] Here, we demonstrated that paclitaxel treatment increased the expression of DDIT4‐AS1, and silencing DDIT4‐AS1 inhibited autophagy, thereby sensitizing TNBC cells to paclitaxel, suggesting that inhibition of DDIT4‐AS1 may be a potential therapeutic strategy to enhance the efficacy of paclitaxel for TNBC patients. Here, DDIT4 is linked to cancer.