Multiple mechanisms underlie this resistance, including aberrant gene expression, activation or hyperactivation of key signaling pathways (such as NF-κB, HIF-1, and PI3K/Akt), epithelial–mesenchymal transition (EMT), the influence of the tumor microenvironment, and the presence of highly resistant cancer stem cells (Notch pathway) [10]. This evidence concerns the gene AKT1 and neoplasm.