It is commonly used to treat ER+ and HER‐ breast cancer, but its efficacy in BLBC is not ideal.[52, 53] It has been reported that knockdown of ACAA1 can increase the anti‐tumor activity of CDK4/6 inhibitors in BLBC.[53] Mechanistically, the synergistic effect of ACAA1 knockdown and CDK4/6 inhibitors reduces the phosphorylation of RB1 and increases the tumor suppressor function of RB1.[53] Our results reveal that KLF5 can promote BLBC cell proliferation by increasing the expression of both Cyclin D1 and XPO1, which increases RB1 phosphorylation and reduces RB1 nuclear localization (Figure 4). This evidence concerns the gene ESR1 and breast carcinoma.