AKT1 and breast cancer: Activation of c-Abl and STAT3 (Hung et al., 2016[16]), NF-κB and Notch1 (Park et al., 2014[32]), cyclin D1 and cdk2 (Kim et al., 2010[21]), or PI3K/AKT and TGF-β (Soncini et al., 2014[38]) has been shown to be responsible for visfatin-mediated BC growth and metastatic potential.