AKT1 and breast cancer: For instance, BCAR4-induced tamoxifen resistance depends on the presence of ERBB2 (HER-2) and ERBB3 receptors [21]; H19 could enhance breast cancer cell proliferation and migration by activating Akt and Erk [22]; HOTAIR could interact with PRC2 to reprogram chromatin states in epigenetic gene silencing to promote cancer migration [23]; further, CASC7 suppressed malignant behaviors of breast cancer by regulating miR-21-5p/FASLG axis [13].