AKT1 and colorectal carcinoma: They also modulate AKT/protein kinase B, involved in cell proliferation, survival, and growth, through its effect on the TSC1/TSC2, mTORC, MAPK, and glucose metabolism [20] pathways that participate in the amplification of molecules favoring cell proliferation, growth, and survival and may explain resistance to first-line treatments in CRC, such as irinotecan, 5-fluorouracil (5-FU), and cisplatin [21].