Importantly, our results displayed the accumulation of autophagy-associated proteins (P62, Beclin 1, and LC3) in sEVs secreted by breast cancer cells treated with MA, but they were attenuated in sEVs derived from RIP1-transfected MDA-MB-231 and MCF-7 cells, indicating that autophagosomes can fuse with either lysosomes or MVBs, and further suggesting that the release of sEVs may compensate for lysosomal dysfunction. Here, MAP1LC3A is linked to breast carcinoma.