**2. KRAS gene**

The most important oncogene for several types of cancer is KRAS. Cytogenetic location of this gene is 12p12.1 [the short (p) arm of chromosome 12 at position 12.1] [10]. The KRAS gene belongs to the Ras family of oncogenes. RAS family oncogenes also include two other genes: H-RAS and N-RAS. These proteins play important roles in cell division, cell differentiation, and apoptotic cell death. KRAS causes the initiation of cancer through deregulation of the G1 cell cycle [10].

The KRAS gene expresses a protein called "K-Ras," which is part of a signaling pathway known as "the RAS/microtubule-associated protein (MAP) kinase signaling (MAPK) pathway." The protein carries the mitogenic signals from the "epidermal growth factor receptor (EGFR)" on the cell surface to the cell nucleus. These signals provide instructions for growth, proliferation, maturation, or differentiation to the cell. The K-Ras protein converts a molecule called guanosine-5′-triphosphate (GTP) into another molecule called guanosine-5′-diphosphate (GDP), and therefore, it is a "GTPase." By such conversion, K-Ras protein almost acts like a "switch," which is turned on and off by the GTP and GDP molecules. In order to transmit signals, K-Ras must bind to GTP, and this turns on the protein [10]. However, K-Ras protein is inactivated when it converts the GTP to GDP. This means that when this particular protein is bound to GDP, it does not send signals to the nucleus. In several pathological conditions [cardiofaciocutaneous syndrome, Noonan syndrome, Costello syndrome, autoimmune lymphoproliferative syndrome (ALPS), and epidermal nevus] and different cancers [colorectal (CRC), pancreatic (PC), and lung cancer; cholangiocarcinoma; and core binding factor acute myeloid leukemia (CBF-AML)], KRAS mutations are observed in patients [10].
