Andrew, a 45 year old patient with a secluded past of alcohol abuse and a preceding diagnosis of mild cirrhosis, presented himself for an initial primary care appointment; after having been absconded from follow up for a 3 year period. He complained of having a loss in energy, and weight within a short period of time. Additionally he was constantly having itchy skin, swollen ankles, and had been noticing blood in his stool for a period of two days which raised his concern. He has a paternal family history of diabetes, which could increase his predisposition to the disease. His mother and aunt suffer from obesity which is a common cause of diabetes. These genetic associations raise a concern that he might easily be affected by obesity-related diseases. Obesity increases the stress to the endoplasmic reticulum, a membranous network in the human cell, which then results in a nerve signal from the ER to the cell. This signal reduces the production of insulin. When this occurs there is an accumulation of high glucose contents in the blood stream, which won't properly be converted to glycogen. Over time, this can then result in liver failure. The first test ordered was a CT scan for screening his liver, due to his medical history. The scan identified a 4.0cm mass which was situated in the right lobe of his liver. The mass was hyperenhancing on another arterial phase, which also had initial washouts on the portal venous phase. His alpha fetoprotein appeared to be raised to abnormal conditions at around 180. Nonetheless, a physical examination was conducted which attributed some of his postulated symptoms directly to the mass in his liver, or to possible liver failure. He was sent to the lab, where he had a blood tests done. The tests were significant for a platelet count of 150. He also had normal levels of creatine, a bilirubin level of 0.8, an INR of 1.1, an AST of 35, and an ALT level of 55. To make sure the patient understood the cause