It was reported that continuous TGF‐β exposure induced breast cancer cell autophagy and proteolytic degradation of Disabled‐2.34 This process was mediated by cathepsin B. In human cardiac fibroblasts, TGF‐β1 promotes fibrogenesis and autophagic activation.35 In the present study, SPHK1 was upregulated by TGF‐β1 treatment, and the pivotal role of SPHK1 in TGF‐β1‐induced HPMCs autophagy was confirmed by depleting SPHK1 in HPMCs. This evidence concerns the gene TGFB1 and breast carcinoma.