Chronic hepatitis C virus (HCV) infection is a public health issue which effects people throughout the world, with more than 71 million people effected, and 400,000 deaths annually (1). HCV, which is when active carriage of HCV RNA is in the blood, is the leading cause of cirrhosis, liver failure, and hepatocellular carcinoma (HCC) (2). Among HCV infected cirrhotic patients, the incidence rate of HCC steadily increases with increased degree of fibrosis, with annual reported incidence of 1.4% to 7% respectively (3). The eradication of the virus and therefore prevention of HCC development and liver related death is the ultimate treatment objective for chronic HCV. In 1991, the first treatment approved by the Food & Drug Administration (FDA) to treat chronic hepatitis C (CHC) was IFNα-2b monotherapy (4), which allowed 15-20% of sustained virological response (SVR) and also induced major side effects such as asthenia, neutropenia, myalgia and influenza-like syndromes (5). In 1998, SVR rates increased to 38% in IFNα-2b and daily oral administration of ribavirin (RBV) combination treated patients (6). In 2001 and 2002, the FDA approved pegylated-IFN (PEG-IFN)α-2b and PEG-IFNα-2a respectively, which allowed IFN-based treatment to be administered weekly. The combination of PEG-IFNα-2a or PEG-IFNα-2b and ribavirin allowed SVR in 56% and 54% of treated patients (7). This regimen given for 6 to 12 months depending on the HCV genotype became the new standard of care (4). After 10 years of stagnation with PEG-IFN/RBV combination, a desirable change spread over several stages. The first stage in 2011 was observed with the launch of the first direct-acting antiviral agents (DAAs). More than 75% of patients infected with HCV