Based on our mechanistic findings, we evaluated the significance of p4E-BP1T37/46 and p62 as biomarkers, which reliably indicated mTORC1-mediated autophagy deficiency in Alpelisib-resistant (Fig. 6g, h) and mTORC1-independent autophagy defects in CRISPR-Cas9-engineered ATG7-knockout BC xenografts (Fig. 7g, h) via immunohistochemical analysis. Here, ATG7 is linked to breast cancer.