AKT1 and breast cancer: MDSCs of a particular phenotype, with a polymorphonuclear structure and neutrophils in bone marrow were reported to mediate doxorubicin resistance through the secretion of soluble factors [71] including IL-1β, which was shown to activate PI3K/Rac and IL-1RI/β-catenin-dependent BIRC3 transcription in breast cancer cells, and CXCL1/GROα which increased angiogenesis in a mouse model of breast cancer [72, 73].