MAP1LC3A and breast cancer: Hypothesizing that the varied response of T47DPar and Alpelisib-resistant subclones to DCA/Metformin reflects mTORC1-dependent differences in autophagic flux, we performed LC3 turnover assays.48 To precisely measure LC3 protein levels, we utilized a HiBiT-tagged LC3, which yields robust and quantitative luminescence via high-affinity interaction with NanoLuc.49 In support of an autophagy defect in Alpelisib-resistant BC cells, we observed a dose-dependent decrease in LC3 HiBiT levels under treatment with Metformin or DCA specifically in T47DPar cells (Fig. 3b, upper panel).