In contrast to MDA-MB-231 breast cancer cells in which COPB2 depletion induced cell death, abortive autophagy and ER stress, COPB2 knock down in MCF10A cells had modest effect on viability, induced autophagic flux and did not increase ER stress (Fig, S9B–D), indicating a therapeutic opportunity if inhibitors targeting one or more of the components of COPI can be developed. This evidence concerns the gene COPB2 and breast cancer.