AKT1 and breast carcinoma: In ovarian and breast cancer, for example, HOTAIR overexpression has been linked to resistance to cisplatin and doxorubicin through activation of the Wnt/β-catenin and PI3K/AKT pathways, by favoring overexpression of β-catenin and maintaining sustained signaling of PI3K/AKT/mTOR pathway effectors, respectively [13,14].