Because ERα interacts with the α-catalytic subunit of the central energy sensor AMP-activated protein kinase (AMPK),61 whereas the substrate accumulation but not end-product depletion of fatty acids from FASN inhibition triggers AMPK activation,62, 63 our findings might implicate de novo lipogenesis operating as a bona fide metabolic signal transmitter,64 regulating breast cancer cell sensitivity not only to E2 but also to antiestrogen therapies.65, 66. This evidence concerns the gene ESR1 and breast cancer.