Tumor cells exhibit a distinctive metabolism in contrast to that of normal cells, not only energy production dependent on aerobic glycolysis but also dysregulated cellular signaling and machinery, increased fatty acid synthesis and glutaminolysis are obviously observed. (Y Zhao et al. 2013) Simultaneously, intrinsic and extrinsic molecular mechanisms have been modified, in order to alter cellular metabolism to meet the nutrient demand in the rapid growth of tumor cells, commonly carbohydrates, proteins, lipids and nucleic acid are the essential sources that cancer cells need to support their growth and division. Previous studies have highlighted metabolic phenotypes of cancer, and the Warberg effect appears to be an important feature. Tumor cells would switch the shunt of ATP production from oxidative phosphorylation to glycolysis even under anaerobic conditions. This effect is regulated by PI3K, hypoxia-inducible factor (HIF), p53, and hepatic AMP-activated kinase B1 (LKB1) pathway. However, adaptation to a new microenvironment as a cellular remodeling process is intended to meet the needs of tumor cells in both macromolecular synthesis and maintenance of redox balance. In the rapid proliferation phase, NADPH and high levels of reactive oxygen species (ROS) are the key molecules that distinguish between tumor cells and normal cells. Importantly, genetic alterations that influence metabolic change are commonly found in oncogenes and mutations of tumor suppressor genes that influence the intracellular cell. signaling routes. These changes can alter metabolism and reengineer the process facilitating the rapid growth and survival of tumor cells through the RAS and mTORC1 pathway. (Rob A. Cairns. et al. 2001 and Chi V Dang. 2012)Lipids, proteins......at the center of the article......complex mechanisms of each type of cancer, can be different in detail and you may need to know more. It would be helpful to adopt the comprehensible approach of melanoma modality studies to the ASS-negative cancer type that has the high prevalence in Thailand, HCC and cholangiocarcinoma (CCA). Beyond the complicated mechanisms of tumor cells, it is interesting to note that ADI treatment combines with other chemotherapy to improve the results of treatment that aims to destroy cancer in a synergistic manner. This is an interesting point to make since the cancer has modified itself to avoid the effects of the drug over time. Thus forcing the cancer to change towards apoptosis and reducing the resistance that may occur later. These details of mechanisms should have been studied thoroughly to provide a solution for cancer treatment to be successful.