AKT1 and cancer: Due to mutations in different genes (PTEN and PI3KCA, etc.)or constitutive activation of different receptor tyrosine kinases (RTKs) (i.e., epidermal growth factor receptor (EGFR), platelet-derived growth factor receptor, and fibroblast growth factor receptor), persistent activation of PI3K-Akt signaling is often detected in CRC [40–43], which is essential for cancer cell growth, proliferation, metastases, as well as metabolism reprogramming and apoptosis/therapy resistances [44].