We grew MCF-7 cells and treated them with the following: (1) CRISPRa-UCP1-AAV adipocytes at the top layer of a Transwell model; (2) 6-aminonicotinamide, which is known to target glycolysis and reduce cell growth in a variety of tumors40–42, including MCF-7 breast cancer cells41, using similar or higher drug concentrations (50 μM, 100 μM and dimethylsulfoxide (DMSO) as a control)41; and (3) etomoxir, an inhibitor of FAO43 that suppresses tumor cell growth44,45, including breast cancer46,47, using concentrations previously used for MCF-7 cells (100 μM, 200 μM and DMSO as a control)47. Here, UCP1 is linked to neoplasm.