According to protein profiling in the human liver biopsies of HCV patients, a correlation was initially discovered between dysfunctional mitochondrial processes, which include beta-oxidation, and HCV. As a matter of fact, lipids play an important role in the replication cycle of HCV, and in the "in vivo" samples from HCV patients, many lipids were found in abundance to aid HCV in virus uptake, RNA replication, and secretion from host cells. Enzymes that regulate fatty acid metabolism, including enoyl-CoA isomerase, were also similarly upregulated. Gene silencing techniques revealed that enoyl-CoA isomerase is essential in HCV RNA replication, and opened ways to stop HCV infection on an intracellular level.