In this study, we validated that defective autophagy induced by SAT1 promoted TNBC progression, which is consistent with previous conclusions that the autophagic capacity of breast cancer cells, especially TNBC tumors, may be impaired at basal levels or after exposure to various stresses.[41, 42, 43] In addition, autophagy‐deficient TNBC cells were found to trigger mTOR mRNA stabilization enabled by m5C modification, which was completed by YBX1. Here, SAT1 is linked to breast carcinoma.