BAZ1B silencing caused significant inhibition of cell proliferation and ERα expression, as well as transcriptome changes resulting in inhibition of estrogen, myc, mTOR, PI3K and AKT signaling and metabolic pathways in AE-sensitive and AE-resistant BC cells, revealing a novel therapeutic vulnerability of these cancer cells via inhibition of BAZ1B. This evidence concerns the gene AKT1 and breast cancer.