AKT1 and breast carcinoma: For example, as extensively reviewed by Varinska et al. (2015), by interfering with the activity of various proangiogenic mediators including VEGF, epithelial growth factor receptor (EGFR), MMPs, nuclear factor-kappa B (NF-κB), phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PI3K/Akt), and GEN (ERK1/2) signaling pathways, GEN strongly inhibited angiogenesis in human breast cancer (BC) [70].